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C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 pathway as a therapeutic target and regulatory mechanism for spinal cord injury
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作者 Xiangzi Wang Xiaofei Niu +4 位作者 Yingkai Wang Yang Liu Cheng Yang Xuyi Chen Zhongquan Qi 《Neural Regeneration Research》 SCIE CAS 2025年第8期2231-2244,共14页
Spinal cord injury involves non-reversible damage to the central nervous system that is characterized by limited regenerative capacity and secondary inflammatory damage.The expression of the C-C motif chemokine ligand... Spinal cord injury involves non-reversible damage to the central nervous system that is characterized by limited regenerative capacity and secondary inflammatory damage.The expression of the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis exhibits significant differences before and after injury.Recent studies have revealed that the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis is closely associated with secondary inflammatory responses and the recruitment of immune cells following spinal cord injury,suggesting that this axis is a novel target and regulatory control point for treatment.This review comprehensively examines the therapeutic strategies targeting the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis,along with the regenerative and repair mechanisms linking the axis to spinal cord injury.Additionally,we summarize the upstream and downstream inflammatory signaling pathways associated with spinal cord injury and the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis.This review primarily elaborates on therapeutic strategies that target the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis and the latest progress of research on antagonistic drugs,along with the approaches used to exploit new therapeutic targets within the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis and the development of targeted drugs.Nevertheless,there are presently no clinical studies relating to spinal cord injury that are focusing on the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis.This review aims to provide new ideas and therapeutic strategies for the future treatment of spinal cord injury. 展开更多
关键词 apoptosis C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 pathway C-C motif chemokine receptor 2 antagonists chemokine ligand 2 chemokine receptor 2 inflammation macrophage microglia spinal cord injury therapeutic method
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Calculus bovis inhibits M2 tumor-associated macrophage polarization via Wnt/β-catenin pathway modulation to suppress liver cancer 被引量:11
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作者 Zhen Huang Fan-Ying Meng +12 位作者 Lin-Zhu Lu Qian-Qian Guo Chang-Jun Lv Nian-Hua Tan Zhe Deng Jun-Yi Chen Zi-Shu Zhang Bo Zou Hong-Ping Long Qing Zhou Sha Tian Si Mei Xue-Fei Tian 《World Journal of Gastroenterology》 SCIE CAS 2024年第29期3511-3533,共23页
BACKGROUND Calculus bovis(CB),used in traditional Chinese medicine,exhibits anti-tumor effects in various cancer models.It also constitutes an integral component of a compound formulation known as Pien Tze Huang,which... BACKGROUND Calculus bovis(CB),used in traditional Chinese medicine,exhibits anti-tumor effects in various cancer models.It also constitutes an integral component of a compound formulation known as Pien Tze Huang,which is indicated for the treatment of liver cancer.However,its impact on the liver cancer tumor microenvironment,particularly on tumor-associated macrophages(TAMs),is not well understood.AIM To elucidate the anti-liver cancer effect of CB by inhibiting M2-TAM polarization via Wnt/β-catenin pathway modulation.METHODS This study identified the active components of CB using UPLC-Q-TOF-MS,evaluated its anti-neoplastic effects in a nude mouse model,and elucidated the underlying mechanisms via network pharmacology,transcriptomics,and molecular docking.In vitro assays were used to investigate the effects of CB-containing serum on HepG2 cells and M2-TAMs,and Wnt pathway modulation was validated by real-time reverse transcriptase-polymerase chain reaction and Western blot analysis.RESULTS This study identified 22 active components in CB,11 of which were detected in the bloodstream.Preclinical investigations have demonstrated the ability of CB to effectively inhibit liver tumor growth.An integrated approach employing network pharmacology,transcriptomics,and molecular docking implicated the Wnt signaling pathway as a target of the antineoplastic activity of CB by suppressing M2-TAM polarization.In vitro and in vivo experiments further confirmed that CB significantly hinders M2-TAM polarization and suppresses Wnt/β-catenin pathway activation.The inhibitory effect of CB on M2-TAMs was reversed when treated with the Wnt agonist SKL2001,confirming its pathway specificity.CONCLUSION This study demonstrated that CB mediates inhibition of M2-TAM polarization through the Wnt/β-catenin pathway,contributing to the suppression of liver cancer growth. 展开更多
关键词 Calculus bovis M2 tumor-associated macrophage polarization Liver cancer Wnt/β-catenin pathway Tumor microenvironment
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Hypoglycemic mechanism of Tegillarca granosa polysaccharides on type 2 diabetic mice by altering gut microbiota and regulating the PI3K-akt signaling pathwaye 被引量:2
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作者 Qihong Jiang Lin Chen +5 位作者 Rui Wang Yin Chen Shanggui Deng Guoxin Shen Shulai Liu Xingwei Xiang 《Food Science and Human Wellness》 SCIE CSCD 2024年第2期842-855,共14页
Type 2 diabetes mellitus(T2DM)is a complex metabolic disease threatening human health.We investigated the effects of Tegillarca granosa polysaccharide(TGP)and determined its potential mechanisms in a mouse model of T2... Type 2 diabetes mellitus(T2DM)is a complex metabolic disease threatening human health.We investigated the effects of Tegillarca granosa polysaccharide(TGP)and determined its potential mechanisms in a mouse model of T2DM established through a high-fat diet and streptozotocin.TGP(5.1×10^(3) Da)was composed of mannose,glucosamine,rhamnose,glucuronic acid,galactosamine,glucose,galactose,xylose,and fucose.It could significantly alleviate weight loss,reduce fasting blood glucose levels,reverse dyslipidemia,reduce liver damage from oxidative stress,and improve insulin sensitivity.RT-PCR and Western blotting indicated that TGP could activate the phosphatidylinositol-3-kinase/protein kinase B signaling pathway to regulate disorders in glucolipid metabolism and improve insulin resistance.TGP increased the abundance of Allobaculum,Akkermansia,and Bifidobacterium,restored the microbiota abundance in the intestinal tracts of mice with T2DM,and promoted short-chain fatty acid production.This study provides new insights into the antidiabetic effects of TGP and highlights its potential as a natural hypoglycemic nutraceutical. 展开更多
关键词 Tegillarca granosa polysaccharide Type 2 diabetes mellitus Glycolipid metabolism PI3K/Akt signaling pathway
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Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway,and induces senescence in hepatocellular carcinoma 被引量:1
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作者 XUEGANG YANG XIANHONG XIANG +3 位作者 GUOHUI XU SHI ZHOU TIANZHI AN ZHI HUANG 《Oncology Research》 SCIE 2024年第1期213-226,共14页
Hepatocellular carcinoma(HCC),a common malignancy worldwide,still lacks effective clinical treatment.The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms.In our... Hepatocellular carcinoma(HCC),a common malignancy worldwide,still lacks effective clinical treatment.The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms.In our study,we initially confirmed a higher level of PRDX2 in the bile of HCC patients compared to those with choledocholithiasis by 2-DE,LC-MS,and ELISA.Subsequently,we demonstrated the high expression of peroxiredoxin 2(PRDX2)in HCC based on the TCGA database and clinical sample analysis.Furthermore,PRDX2 overexpression enhanced the viability of HCC cells.And PRDX2 silencing induced senescence of HCC cells.In vivo,knockdown of PRDX2 significantly reduced the weight of xenograft tumors.PRDX2 also was found to activate the Wnt/β-catenin pathway by inducingβ-catenin nuclear translocation.Consequently,we proved that silencing PRDX2 could inhibit proliferation and Wnt/β-catenin pathway while promoting senescence in HCC cells. 展开更多
关键词 Peroxiredoxin 2 Hepatocellular carcinoma Wnt/β-catenin pathway SENESCENCE PROLIFERATION
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High glucose causes apoptosis of rabbit corneal epithelial cells involving activation of PERK-eIF2α-CHOP-caspase-12 signaling pathway 被引量:7
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作者 Pan-Pan Yao Min-Jie Sheng +6 位作者 Wen-Hao Weng Yin Long Hao Liu Li Chen Jia-Jun Lu Ao Rong Bing Li 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2019年第12期1815-1822,共8页
AIM: To investigate the effect of high concentration of glucose(HCG) on double stranded RNA-activated protein kinase-like ER kinase(PERK)-eukaryotic initiation factor-2α(eIF2α)-transcription factor C/EBP homologous ... AIM: To investigate the effect of high concentration of glucose(HCG) on double stranded RNA-activated protein kinase-like ER kinase(PERK)-eukaryotic initiation factor-2α(eIF2α)-transcription factor C/EBP homologous protein(CHOP)-cysteine aspartate specific proteinase(caspase-12) signaling pathway activation and apoptosis in rabbit corneal epithelial cells(RCECs). METHODS: RCECs were treated by different concentrations of glucose for 0-48 h. The expressions of PERK, p-PERK, eIF2α, p-eIF2α, 78 k Da glucose-regulated protein 78(GRP78), CHOP, B-cell lymphoma 2(Bcl-2), B-cell lymphoma-2-associated X protein(Bax) and caspase-12 were determined by Western blot. Apoptosis was detected by TUNEL assay. Meanwhile, the function of PERK-eI F2α-CHOP-caspase-12 signaling pathway activation in high glucose-induced apoptosis was evaluated using PERK inhibitor, GSK2606414. RESULTS: HCG significantly promoted the expression of p-PERK, p-eIF2α, GRP78, CHOP, Bax and cleaved caspase-12 in RCECs(P<0.05), while remarkably decreased the expression of Bcl-2 and caspase-12(P<0.05), and the alterations caused by glucose were in concentration-and time-dependent manners. Meanwhile, PERK and eIF2α expressions were not affected in all groups(P>0.05). TUNEL assay showed that the apoptosis rate of RCECs in the HCG group increased significantly in contrast with that in the normal concentration of glucose or osmotic pressure control group(P<0.05), and the apoptosis rate increased with the increase of glucose concentration within limits(P<0.05). GSK2606414 down-regulated the expression of p-PERK and p-eI F2α in the HCG group(P<0.05), while still did not affect the expression of PERK and eIF2α among groups(P>0.05). Correspondingly, GSK2606414 also significantly reduced the apoptosis rate induced by high glucose(P<0.05). CONCLUSION: HCG activates PERK-eIF2α-CHOPcaspase-12 signaling pathway and promotes apoptosis of RCECs. 展开更多
关键词 high glucose rabbit corneal epithelial cells perk-eif2α-CHOP-caspase-12 pathway APOPTOSIS
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Protective effects of sodium butyrate on rotavirus inducing endoplasmic reticulum stress-mediated apoptosis via PERK-eIF2αsignaling pathway in IPEC-J2 cells 被引量:4
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作者 Ye Zhao Ningming Hu +11 位作者 Qin Jiang Li Zhu Ming Zhang Jun Jiang Manyi Xiong Mingxian Yang Jiandong Yang Linyuan Shen Shunhua Zhang Lili Niu Lei Chen Daiwen Chen 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2021年第4期1543-1554,共12页
Background:Rotavirus(RV)is a major pathogen that causes severe gastroenteritis in infants and young animals.Endoplasmic reticulum(ER)stress and subsequent apoptosis play pivotal role in virus infection.However,the pro... Background:Rotavirus(RV)is a major pathogen that causes severe gastroenteritis in infants and young animals.Endoplasmic reticulum(ER)stress and subsequent apoptosis play pivotal role in virus infection.However,the protective mechanisms of intestinal damage caused by RV are poorly defined,especially the molecular pathways related to enterocytes apoptosis.Thus,the aim of this study was to investigate the protective effect and mechanism of sodium butyrate(SB)on RV-induced apoptosis of IPEC-J2 cells.Results:The RV infection led to significant cell apoptosis,increased the expression levels of ER stress(ERS)markers,phosphorylated protein kinase-like ER kinase(PERK),eukaryotic initiation factor 2 alpha(eIF2α),caspase9,and caspase3.Blocking PERK pathway using specific inhibitor GSK subsequently reversed RV-induced cell apoptosis.The SB treatment significantly inhibited RV-induced ERS by decreasing the expression of glucose regulated protein 78(GRP78),PERK,and eIF2α.In addition,SB treatment restrained the ERS-mediated apoptotic pathway,as indicated by downregulation of C/EBP homologous protein(CHOP)mRNA level,as well as decreased cleaved caspase9 and caspase3 protein levels.Furthermore,siRNA-induced GPR109a knockdown significantly suppressed the protective effect of SB on RV-induced cell apoptosis.Conclusions:These results indicate that SB exerts protective effects against RV-induced cell apoptosis through inhibiting ERS mediated apoptosis by regulating PERK-eIF2αsignaling pathway via GPR109a,which provide new ideas for the prevention and control of RV. 展开更多
关键词 Apoptosis IPEC-J2 perk-eif2α ROTAVIRUS Sodium butyrate
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Reduction of the oxidative damage to H_(2)O_(2)-induced HepG2 cells via the Nrf2 signalling pathway by plant flavonoids Quercetin and Hyperoside
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作者 Meijing Zhang Gaoshuai Zhang +10 位作者 Xiangxing Meng Xinxin Wang Jiao Xie Shaoshu Wang Biao Wang Jilite Wang Suwen Liu Qun Huang Xu Yang Jing Li Hao Wang 《Food Science and Human Wellness》 SCIE CAS CSCD 2024年第4期1864-1876,共13页
Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pat... Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pathway predicted by network pharmacology.And the antioxidant effect and mechanism of hyperoside and quercetin were measured and compared in H_(2)O_(2)-induced Hep G2 cells and Caenorhabditis elegans.The findings indicated that quercetin was more effective than hyperoside in reducing oxidative damage,which was proved by improved cell viability,decreased reactive oxygen species(ROS)production,decreased cellular apoptosis,and alleviated mitochondrial damage.In addition,quercetin was more efficient than hyperoside in enhancing the expression of Nrf2-associated m RNAs,increasing the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT),and reducing the cellular malondialdehyde(MDA)content.Quercetin was superior to hyperoside in prolonging the lifespan of worms,decreasing the accumulation of lipofuscin,inhibiting ROS production,and increasing the proportion of skn-1 in the nucleus.With the Nrf2 inhibitor ML385,we verified that quercetin and hyperoside primarily protected the cells against oxidative damage via the Nrf2 signalling pathway.Furthermore,molecular docking and dynamics simulations demonstrated that the quercetin-Kelch-like ECH-associated protein 1(Keap1)complex was more stable than the hyperoside-Keap1 complex.The stable structure of the complex might hinder the binding of Nrf2 and Keap1 to release Nrf2 and facilitate its entry into the nucleus to play an antioxidant role.Overall,quercetin had a better antioxidant than hyperoside. 展开更多
关键词 HYPEROSIDE QUERCETIN HepG2 cell Oxidative damage Nrf2 signalling pathway
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Hesperidin ameliorates H_(2)O_(2)-induced bovine mammary epithelial cell oxidative stress via the Nrf2 signaling pathway
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作者 Qi Huang Jiashuo Liu +2 位作者 Can Peng Xuefeng Han Zhiliang Tan 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2024年第4期1737-1750,共14页
Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucid... Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucidated.Results In this study, we investigated the effects of hesperidin on H_(2)O_(2)-induced oxidative stress in b MECs and the underlying molecular mechanism. We found that hesperidin attenuated H_(2)O_(2)-induced cell damage by reducing reactive oxygen species(ROS) and malondialdehyde(MDA) levels, increasing catalase(CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.Conclusions Our results suggest that hesperidin could protect b MECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary. 展开更多
关键词 Bovine mammary epithelial cell HESPERIDIN Nrf2 signaling pathway Oxidative stress
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“Baihui”(DU20)-penetrating “Qubin”(GB7) acupuncture on blood–brain barrier integrity in rat intracerebral hemorrhage models via the RhoA/ROCK Ⅱ/MLC 2 signaling pathway
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作者 Ce Zhang Jia Zheng +10 位作者 Xueping Yu Binglin Kuang Xiaohong Dai Lei Zheng Weiwei Yu Wei Teng Hongtao Cao Mingyue Li Jiayong Yao Xiaoying Liu Wei Zou 《Animal Models and Experimental Medicine》 CAS CSCD 2024年第5期740-757,共18页
Background: Blocking the Rho A/ROCK Ⅱ/MLC 2(Ras homolog gene family member A/Rho kinase Ⅱ/myosin light chain 2) signaling pathway can initiate neuroprotective mechanisms against neurological diseases such as stroke,... Background: Blocking the Rho A/ROCK Ⅱ/MLC 2(Ras homolog gene family member A/Rho kinase Ⅱ/myosin light chain 2) signaling pathway can initiate neuroprotective mechanisms against neurological diseases such as stroke, cerebral ischemia, and subarachnoid hemorrhage. Nevertheless, it is not clear whether and how disrupting the Rho A/ROCK Ⅱ/MLC 2 signaling pathway changes the pathogenic processes of the blood–brain barrier(BBB) after intracerebral hemorrhage(ICH). The present investigation included the injection of rat caudal vein blood into the basal ganglia area to replicate the pathophysiological conditions caused by ICH. Methods: Scalp acupuncture(SA) therapy was performed on rats with ICH at the acupuncture point “Baihui”-penetrating “Qubin,” and the ROCK selective inhibitor fasudil was used as a positive control to evaluate the inhibitory effect of acupuncture on the Rho A/ROCK Ⅱ/MLC 2 signaling pathway. Post-assessments included neurological deficits, brain edema, Evans blue extravasation, Western blot, quantitative polymerase chain reaction, and transmission electron microscope imaging. Results: We found that ROCK Ⅱ acts as a promoter of the Rho A/ROCK Ⅱ/MLC 2 signaling pathway, and its expression increased at 6 h after ICH, peaked at 3 days, and then decreased at 7 days after ICH, but was still higher than the preintervention level. According to some experimental results, although 3 days is the peak, 7 days is the best time point for acupuncture treatment. Starting from 6 h after ICH, the neurovascular structure and endothelial cell morphology around the hematoma began to change. Based on the changes in the promoter ROCK Ⅱ, a 7-day time point was selected as the breakthrough point for treating ICH model rats in the main experiment. The results of this experiment showed that both SA at “Baihui”-penetrating “Qubin” and treatment with fasudil could improve the expression of endothelial-related proteins by inhibiting the Rho A/ROCK Ⅱ/MLC 2 signaling pathway and reduce neurological dysfunction, brain edema, and BBB permeability in rats. Conclusion: This study found that these experimental data indicated that SA at “Baihui”-penetrating “Qubin” could preserve BBB integrity and neurological function recovery after ICH by inhibiting Rho A/ROCK Ⅱ/MLC 2 signaling pathway activation and by regulating endothelial cell–related proteins. 展开更多
关键词 blood-brain barrier CAVEOLAE INTRACEREBRAL hemorrhage RhoA/ROCK II/MLC 2 signaling pathway SCALP ACUPUNCTURE
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Enhancement of porcine in vitro embryonic development through luteolin‑mediated activation of the Nrf2/Keap1 signaling pathway
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作者 Se-Been Jeon Pil-Soo Jeong +5 位作者 Min Ju Kim Hyo-Gu Kang Bong-Seok Song Sun-Uk Kim Seong-Keun Cho Bo-Woong Sim 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2024年第2期600-613,共14页
Background Oxidative stress,caused by an imbalance in the production and elimination of intracellular reactive oxygen species(ROS),has been recognized for its detrimental effects on mammalian embryonic development.Lut... Background Oxidative stress,caused by an imbalance in the production and elimination of intracellular reactive oxygen species(ROS),has been recognized for its detrimental effects on mammalian embryonic development.Luteolin(Lut)has been documented for its protective effects against oxidative stress in various studies.However,its specific role in embryonic development remains unexplored.This study aims to investigate the influence of Lut on porcine embryonic development and to elucidate the underlying mechanism.Results After undergoing parthenogenetic activation(PA)or in vitro fertilization,embryos supplemented with 0.5μmol/L Lut displayed a significant enhancement in cleavage and blastocyst formation rates,with an increase in total cell numbers and a decrease in the apoptosis rate compared to the control.Measurements on D2 and D6 revealed that embryos with Lut supplementation had lower ROS levels and higher glutathione levels compared to the control.Moreover,Lut supplementation significantly augmented mitochondrial content and membrane potential.Intriguingly,activation of the Nrf2/Keap1 signaling pathway was observed in embryos supplemented with Lut,leading to the upregulation of antioxidant-related gene transcription levels.To further validate the relationship between the Nrf2/Keap1 signaling pathway and effects of Lut in porcine embryonic development,we cultured PA embryos in a medium supplemented with brusatol,with or without the inclusion of Lut.The positive effects of Lut on developmental competence were negated by brusatol treatment.Conclusions Our findings indicate that Lut-mediated activation of the Nrf2/Keap1 signaling pathway contributes to the enhanced production of porcine embryos with high developmental competence,and offers insight into the mechanisms regulating early embryonic development. 展开更多
关键词 LUTEOLIN Mitochondrial function Nrf2/Keap1 signaling pathway Oxidative stress Porcine embryo development
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IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway
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作者 ZIYONG LIU TAO MA +2 位作者 JINFANG LI WEI REN ZHIXIN ZHANG 《Oncology Research》 SCIE 2024年第9期1453-1465,共13页
Background:Interleukin 13 receptor subunit alpha 2(IL13RA2)plays an essential role in the progression of many cancers.However,the role of IL13RA2 in infantile haemangioma(IH)is still unknown.Materials and Methods:IL13... Background:Interleukin 13 receptor subunit alpha 2(IL13RA2)plays an essential role in the progression of many cancers.However,the role of IL13RA2 in infantile haemangioma(IH)is still unknown.Materials and Methods:IL13RA2 expression in IH tissues was analyzed using western blot,qRT-PCR,and immunofluorescence.The role of IL13RA2 in haemangioma-derived endothelial cells(HemECs)was determined following knockdown or overexpression of IL13RA2 using CCK-8,colony formation,apoptosis,wound healing,tubule formation,Transwell,and western blot.Results:IL13RA2 expression was upregulated in IH tissues.IL13RA2 overexpression promoted proliferation,migration,and invasion of HemECs and induced glycolysis,which was confirmed with a glycolysis inhibitor.Specifically,IL13RA2 interacted withβ-catenin and activated the Wnt/β-catenin pathway in HemECs,which were involved in the above-mentioned effects of IL13RA2.Conclusions:These findings revealed that targeting IL13RA2 is a potential therapeutic approach for IH. 展开更多
关键词 Infantile haemangioma IL13RA2 GLYCOLYSIS Wnt/β-catenin pathway
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Naringin ameliorates H_(2)O_(2)-induced oxidative damage in cells and prolongs the lifespan of female Drosophila melanogaster via the insulin signaling pathway
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作者 Xiaomei Du Kexin Wang +7 位作者 Xiaoyan Sang Xiangxing Meng Jiao Xie Tianxin Wang Xiaozhi Liu Qun Huang Nan Zhang Hao Wang 《Food Science and Human Wellness》 SCIE CSCD 2024年第3期1231-1245,共15页
Naringin exists in a wide range of Chinese herbal medicine and has proven to possess several pharmacological properties.In this study,PC12,HepG2 cells,and female Drosophila melanogaster were used to investigate the an... Naringin exists in a wide range of Chinese herbal medicine and has proven to possess several pharmacological properties.In this study,PC12,HepG2 cells,and female Drosophila melanogaster were used to investigate the antioxidative and anti-aging effects of naringin and explore the underlying mechanisms.The results showed that naringin inhibited H_(2)O_(2)-induced decline in cell viability and decreased,the content of reactive oxygen species in cells.Meanwhile,naringin prolonged the lifespan of flies,enhanced the abilities of climbing and the resistance to stress,improved the activities of antioxidant enzymes,and decreased malondialdehyde content.Naringin also improved intestinal barrier dysfunction and reduced abnormal proliferation of intestinal stem cells.Moreover,naringin down-regulated the mRNA expressions of inr,chico,pi 3k,and akt-1,and up-regulated the mRNA expressions of dilp2,dilp3,dilp5,and foxo,thereby activating autophagy-related genes and increasing the number of lysosomes.Furthermore,the mutant stocks assays and computer molecular simulation results further indicated that naringin delayed aging by inhibiting the insulin signaling(IIS)pathway and activating the autophagy pathway,which was consistent with the result of network pharmacological predictions. 展开更多
关键词 Drosophila melanogaster Insulin signaling(IIS)pathway NARINGIN PC12 cell HepG2 cell
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COL4A2 enhances thyroid cancer cell proliferation through the AKT pathway
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作者 LIANG HE WEI HAN +1 位作者 KAI YUE XUDONG WANG 《Oncology Research》 SCIE 2024年第9期1467-1478,共12页
Objectives:Thyroid cancer(THCA)is the most common malignant tumor in endocrine system and the incidence has been increasing worldwide.And the number of patients dying from THCA has also gradually risen because the inc... Objectives:Thyroid cancer(THCA)is the most common malignant tumor in endocrine system and the incidence has been increasing worldwide.And the number of patients dying from THCA has also gradually risen because the incidence continues to increase,so the mechanisms related to effective targets is necessary to improve the survival.This study was to preliminarily investigate the effects of the COL4A2 gene on the regulation of thyroid cancer(THCA)cell proliferation and the associated pathways.Methods:Bioinformatics analysis revealed that COL4A2 was closely associated with cancer development.COL4A2 expression in THCA tissues was analyzed using immunohistochemistry,and survival information was determined via Kaplan-Meier curves.The expression of COL4A2 and AKT pathway-related genes were analyzed using qPCR and western blot analyses.Colony formation as well as CCK-8 assays exhibited the cell proliferation level and cell activity,respectively.Downstream of COL4A2 was identified by Gene set enrichment analysis(GSEA).The effects of the COL4A2 and AKT pathways on THCA tumor growth in vivo were determined using a mouse model.Results:Bioinformatics analysis exhibited that COL4A2 plays a significant role in cancer and that the AKT pathway is downstream of COL4A2.THCA patients with high COL4A2 expression had shorter recurrence-free survival.Upregulation of COL4A2 gene expression in 2 THCA cell lines promoted tumor cell growth and activity.The use of AKT pathway blockers also restrained the growth and activity of the 2 THCA cell lines.The use of AKT pathway blockers reduced tumor volume and mass and prolonged mouse survival.Conclusions:COL4A2 can promote the growth as well as development of THCA through the AKT pathway and COL4A2 could be used as a target for THCA. 展开更多
关键词 Thyroid cancer(THCA) PROLIFERATION COL4A2 AKT pathway Biomarker cancer progression
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Inhibition of M2 tumor-associated macrophages polarization by modulating the Wnt/β-catenin pathway as a possible liver cancer therapy method
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作者 Vladislav V Tsukanov Julia L Tonkikh +1 位作者 Edward V Kasparov Alexander V Vasyutin 《World Journal of Gastroenterology》 SCIE CAS 2024年第40期4399-4403,共5页
The problem of liver cancer is becoming increasingly important due to the epi-demic of metabolic diseases and persistent high alcohol consumption.This deter-mines great attention to the development and improvement of ... The problem of liver cancer is becoming increasingly important due to the epi-demic of metabolic diseases and persistent high alcohol consumption.This deter-mines great attention to the development and improvement of methods for early diagnosis and treatment of liver cancer.Huang et al presented a study in the World Journal of Gastroenterology,in which they showed that the use of the traditional Chinese medicine Calculus bovis(CB)can suppress tumor growth in mice by inhibiting M2 tumor-associated macrophages(TAM)through modulating the activity of the Wnt/β-catenin pathway.The interaction of CB components with the Wnt/β-catenin pathway,M2 TAM polarization,and tumor dynamics were studied using network pharmacology,transcriptomics,and molecular docking.It is now generally accepted that the polarization of TAM and the differentiation of the functions of M1 and M2 phagocytes are of great importance for the progression of neoplasms.It is assumed that M2 TAM promote proliferation and migration of tumor cells.Attempts to medicinally influence the Wnt/β-catenin pathway in order to modulate phagocyte polarization now belong to one of the most promising areas of immunotherapy of oncological diseases.Undoubtedly,the work of the Chinese authors deserves attention and further development. 展开更多
关键词 Liver cancer Treatment Calculus bovis Tumor-associated macrophages M2 tumor Macrophage polarization Wnt/β-catenin pathway
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X-Paste improves wound healing in diabetes via NF-E2-related factor/HO-1 signaling pathway
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作者 Ming-Wei Du Xin-Lin Zhu +8 位作者 Dong-Xing Zhang Xian-Zhen Chen Li-Hua Yang Jin-Zhou Xiao Wen-Jie Fang Xiao-Chun Xue Wei-Hua Pan Wan-Qing Liao Tao Yang 《World Journal of Diabetes》 SCIE 2024年第6期1299-1316,共18页
BACKGROUND Diabetic foot ulcers(DFU),as severe complications of diabetes mellitus(DM),significantly compromise patient health and carry risks of amputation and mortality.AIM To offer new insights into the occurrence a... BACKGROUND Diabetic foot ulcers(DFU),as severe complications of diabetes mellitus(DM),significantly compromise patient health and carry risks of amputation and mortality.AIM To offer new insights into the occurrence and development of DFU,focusing on the therapeutic mechanisms of X-Paste(XP)of wound healing in diabetic mice.METHODS Employing traditional Chinese medicine ointment preparation methods,XP combines various medicinal ingredients.High-performance liquid chromatography(HPLC)identified XP’s main components.Using streptozotocin(STZ)-induced diabetic,we aimed to investigate whether XP participated in the process of diabetic wound healing.RNA-sequencing analyzed gene expression differences between XP-treated and control groups.Molecular docking clarified XP’s treatment mechanisms for diabetic wound healing.Human umbilical vein endothelial cells(HUVECs)were used to investigate the effects of Andrographolide(Andro)on cell viability,reactive oxygen species generation,apoptosis,proliferation,and metastasis in vitro following exposure to high glucose(HG),while NF-E2-related factor-2(Nrf2)knockdown elucidated Andro’s molecular mechanisms.RESULTS XP notably enhanced wound healing in mice,expediting the healing process.RNA-sequencing revealed Nrf2 upregulation in DM tissues following XP treatment.HPLC identified 21 primary XP components,with Andro exhibiting strong Nrf2 binding.Andro mitigated HG-induced HUVECs proliferation,metastasis,angiogenic injury,and inflammation inhibition.Andro alleviates HG-induced HUVECs damage through Nrf2/HO-1 pathway activation,with Nrf2 knockdown reducing Andro’s proliferative and endothelial protective effects.CONCLUSION XP significantly promotes wound healing in STZ-induced diabetic models.As XP’s key component,Andro activates the Nrf2/HO-1 signaling pathway,enhancing cell proliferation,tubule formation,and inflammation reduction. 展开更多
关键词 Words:Diabetes mellitus Wound healing NF-E2-related factor-2/HO-1 signaling pathway ANDROGRAPHOLIDE
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Exploring the mechanism of electroacupuncture at different acupoints on acute colitis rats based on JAK2/STAT3/SOCS1 signaling pathway
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作者 ZHANG Chun-qing TANG Kun-peng +2 位作者 YAN Li-ping WEN Tan WANG Hai-jun 《Journal of Hainan Medical University》 CAS 2024年第3期1-7,共7页
Objective:To investigate the mechanism of JAK2/STAT3/SOCS1 signaling pathway in electroacupuncture of different acupoints on acute colitis rats.Methods:36 SPF SD rats were randomly divided into 6 groups,with 6 rats in... Objective:To investigate the mechanism of JAK2/STAT3/SOCS1 signaling pathway in electroacupuncture of different acupoints on acute colitis rats.Methods:36 SPF SD rats were randomly divided into 6 groups,with 6 rats in each group.The rat model of acute colitis was prepared by enema with glacial acetic acid solution.After the model was established,electroacupuncture was given to each acupoint group,with density wave,frequency 2Hz-50 Hz,intensity 2 mA,muscle tremor as the degree 20 min/time,1 time/day,for 3 consecutive days.Observe the general condition of rats;the pathological changes of colonic mucosa in rats were observed by HE method.The contents of serum interleukin-4(IL-4)and interleukin-8(IL-8)were detected by ELISA.Western blot and RT-PCR were used to detect the expression of JAK2,STAT3,SOCS1 protein and mRNA in rat colon tissue.Results:In contrast to the normal group,the overall condition of the model group was worse,the colonic mucosa was severely damaged,even necrotic,and the ulcer surface was obvious.The content of IL-4 in serum was obviously reduced,and the content of IL-8 was obviously go up(P<0.01).The protein content of JAK2,STAT3 and the expression of JAK2,STAT3 mRNA in colon tissue of rats were obviously go up,while the protein content of SOCS1 and the expression of SOCS1 mRNA were obviously reduced(P<0.01).In contrast to the model group,the general condition of rats in each acupoint group was significantly improved,the damage and necrosis of colonic mucosa and ulcer surface were obviously alleviated,the content of IL-4 in serum was obviously go up,and the content of IL-8 was significantly decreased(P<0.01).The protein content of JAK2,STAT3 and the expression of JAK2,STAT3 mRNA in colon tissue of rats were obviously reduced,while the protein content of SOCS1 and the expression of SOCS1 mRNA were obviously go up(P<0.05,P<0.01).Comparison of different acupoint groups,the colonic mucosal injury in the Zusanli group was significantly reduced,the content of serum IL-4 was significantly increased,and the content of IL-8 was significantly decreased(P<0.05,P<0.01).The protein content and mRNA expression of JAK2 and STAT3 in colon tissue were significantly down-regulated,while the protein content and mRNA expression of SOCS1 were significantly go up(P<0.05,P<0.01).Conclusion:Electroacupuncture at each acupoint can improve the damage of colonic mucosa and reduce the inflammatory response.The therapeutic effect of Zusanli(ST36)is better than that of Tianshu(ST25),Dachangshu(BL25)and Shangjuxu(ST37).The mechanism may be related to the regulation of JAK2/STAT3/SOCS1 signaling pathway related proteins and inflammatory cytokines IL-4 and IL-8. 展开更多
关键词 ELECTROACUPUNCTURE Different acupoints Acute colitis Inflammatory factors JAK2/STAT3/SOCS1 signaling pathway
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Oleanolic acid inhibits colon cancer cell stemness and reverses chemoresistance by suppressing JAK2/STAT3 signaling pathway
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作者 RUOYU CHEN YIMAN WU +3 位作者 FENG WANG JUNTAO ZHOU HUAZHANG ZHUANG WEI LI 《BIOCELL》 SCIE 2024年第7期1037-1046,共10页
Background:Oleanolic acid(OA),a pentacyclic triterpenoid exhibiting specific anti-cancer properties and highly effective antioxidant activity,was isolated from traditional Chinese medicinal herbs.Conversely,the OA that... Background:Oleanolic acid(OA),a pentacyclic triterpenoid exhibiting specific anti-cancer properties and highly effective antioxidant activity,was isolated from traditional Chinese medicinal herbs.Conversely,the OA that impacts colon cancer(CC)cells and its underlying mechanisms remain poorly understood.Methods:The cytotoxic effect of OA alone or OA-5-Fluorouracil(5-FU)combination on normal and CC cells was analyzed by methyl thiazolyl diphenyl-tetrazolium bromide(MTT).Then,the impact of OA on CC cell lines(LoVo and HT-29)proliferation and stemness were measured using colon formation and tumorsphere formation assays.Octamer-binding transcription factor 4(Oct4),Prominin-1(CD133),Nanog,and transcription factor SOX-2(SOX2)are cell stemness-related indicators whose expression was assessed usingfluorescence qPCR assay,Western blotting,and immunohistochemistry.The effect of OA on the proliferative potency of CC cells was evaluated using an in vivo model.Results:The stem-like characteristics and clone production of colon cancer cells were markedly reduced by OA alone or in combination with OA-5-FU.Moreover,OA increases the susceptibility of CC cells to 5-FU by blocking the cell stemness-related markers(CD133,Nanog,SOX2,and Oct4)expression levels both in vitro and in vivo,as well as by inactivating the activator of transcription 3(STAT3 signaling)and Janus kinase 2/signal transducer(JAK2).Conclusion:Thesefindings imply that oleanolic acid,both in vitro and in vivo,suppresses the JAK2/STAT3 pathway,which in turn reverses chemoresistance and decreases colon cancer cell stemness.Therefore,by reducing the recommended amount of 5-FU,this strategy may improve chemotherapeutic effectiveness and minimize undesired side effects. 展开更多
关键词 Colon cancer Oleanolic acid Stemness 5-FU JAK2/STAT3 signaling pathway
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Comparative study of anti-inflammatory effects of different processed products through the COX-2/PGE2 signaling pathway: based on network pharmacology and molecular docking
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作者 Ping Chen Yun-Yun Quan +2 位作者 An-Qi Zeng Ying Dai Jin Zeng 《Pharmacology Discovery》 2024年第2期32-45,共14页
Background:Radix Aconiti Lateralis Preparata(Fu-zi)is a traditional Chinese medicinal herb,which has been widely used in the clinic and has potent anti-inflammatory activities.we aimed to explore the mechanisms of ext... Background:Radix Aconiti Lateralis Preparata(Fu-zi)is a traditional Chinese medicinal herb,which has been widely used in the clinic and has potent anti-inflammatory activities.we aimed to explore the mechanisms of extract containing alkaloids from different Fu-zi Processed Products(FPP)in treating inflammation,especially rheumatoid arthritis(RA).Methods:Firstly,using network pharmacology technology,the ingredients,and targets of Fu-zi were obtained by searching and screening,the targets involving RA were acquired,the intersection targets were constructed a"component-target-pathway"network.A comprehensive investigation was conducted on the anti-rheumatoid arthritis mechanisms of 5 FPPs in lipopolysaccharide(LPS)induced RAW264.7 cells,which serve as a model for RA.The production of NO and inflammatory cytokines were measured by ELISA kit.Quantitative Real-time PCR(qRT-PCR)was utilized to measure the mRNA levels.COX-2/PGE2 signaling pathway-associated proteins were determined by western blot.Results:According to a network pharmacological study,16 chemical components and 43 common targets were found in Fu-zi and 6 key targets including PTGS2 were closely related to the mechanism of Fu-zi in treating RA.The in vitro study revealed that the levels of NO,TNF-α,and IL-1βwere substantially decreased by the 5 FPPs.The 5 FPPs significantly suppressed the expression of proteins COX-2,iNOS,and NF-κB,with particularly notable effects observed for PFZ and XFZ.Conclusion:Altogether,these results demonstrated that the 5 PPS containing alkaloids have a good anti-RA-related inflammatory effect,and the mechanism may be related to COX-2/PGE2 signaling pathway,particularly,Fu-zi prepared utilizing a traditional Chinese technique. 展开更多
关键词 Radix Aconiti Lateralis Preparata(Fu-zi) rheumatoid arthritis ANTI-INFLAMMATORY network pharmacology COX-2/PGE2 signaling pathway
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Influence of gut bacteria on type 2 diabetes:Mechanisms and therapeutic strategy
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作者 Xue Wen Lu-Ming Qi Kui Zhao 《World Journal of Diabetes》 SCIE 2025年第1期27-33,共7页
The onset and progression of type 2 diabetes mellitus(T2DM)are strongly associated with imbalances in gut bacteria,making the gut microbiome a new potential therapeutic focus.This commentary examines the recent public... The onset and progression of type 2 diabetes mellitus(T2DM)are strongly associated with imbalances in gut bacteria,making the gut microbiome a new potential therapeutic focus.This commentary examines the recent publication in World Journal of Diabetes.The article explores the association between T2DM and gut microbiota,with a focus on the pathophysiological changes related to dysbiosis.It proposes innovative microbiome-targeted therapeutic strategies and evaluates the challenges and future directions of such approaches.This editorial summarizes the key points of their discussion of the role of the gut microbiome in T2DM and elaborates on the influence of specific gut microbial species on the disease through the host–microbiota metabolic axis.It provides new insights for future research on gut-microbiota-based interventions for T2DM. 展开更多
关键词 Type 2 diabetes Intestinal microbiome Intestinal axis Biological pathways TREATMENT Short-chain fatty acids
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基于PERK-eIF2α信号通路探讨眼针对脑缺血再灌注损伤大鼠脑组织Atg12表达的影响 被引量:3
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作者 赵甲秀 潘茜 +7 位作者 于丹 王莹 邰东梅 马贤德 徐畅 何树诺 张威 王哲 《中华中医药学刊》 CAS 北大核心 2023年第10期60-63,I0013,共5页
目的 通过检测各组脑组织中磷酸化蛋白激酶R样内质网激酶(phosphorylation protein kinase-like ER kinase, p-PERK)、磷酸化真核起始因子2α(phosphorylated α subunit of eukaryotic initiation factor 2,p-eIF2α)、自噬相关基因12(... 目的 通过检测各组脑组织中磷酸化蛋白激酶R样内质网激酶(phosphorylation protein kinase-like ER kinase, p-PERK)、磷酸化真核起始因子2α(phosphorylated α subunit of eukaryotic initiation factor 2,p-eIF2α)、自噬相关基因12(antigen, Atg12)蛋白表达水平的变化,探讨眼针是否能够通过调控内质网应激信号通路PERK-eIF2α影响脑缺血再灌注损伤(cerebral ischemia reperfusion injury, CIRI)大鼠脑组织Atg12的表达。方法 建立大鼠脑缺血再灌注损伤模型,实验分为4组,即:对照组、假手术组、模型组、眼针组。末次针刺后,对各组大鼠进行神经功能缺损评分,透射电镜观察各组大鼠自噬小体的表达情况,然后采用Western blot法检测脑组织中p-PERK、p-eIF2α、Atg12蛋白表达。结果 与对照组和假手术组相比,模型组大鼠神经功能缺损评分、脑组织中p-PERK、p-eIF2α、Atg12蛋白表达均升高,差异具有统计学意义(P<0.01),自噬小体数量增多;与模型组相比,眼针组大鼠神经功能缺损评分、脑缺血组织中p-PERK、p-eIF2α、Atg12的蛋白表达明显降低,差异具有统计学意义(P<0.01),自噬小体数量减少。结论 眼针能够降低脑缺血再灌注损伤模型大鼠脑组织自噬蛋白Atg12的表达,其机制可能与调控内质网应激通路PERK-eIF2α有关。 展开更多
关键词 脑缺血再灌注损伤 眼针疗法 perk-eif2α通路 Atg12
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