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Metformin promotes angiogenesis and functional recovery in aged mice after spinal cord injury by adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway 被引量:3
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作者 Jin-Yun Zhao Xiao-Long Sheng +7 位作者 Cheng-Jun Li Tian Qin Run-Dong He Guo-Yu Dai Yong Cao Hong-Bin Lu Chun-Yue Duan Jian-Zhong Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第7期1553-1562,共10页
Treatment with metformin can lead to the recovery of pleiotropic biological activities after spinal cord injury.However,its effect on spinal cord injury in aged mice remains unclear.Considering the essential role of a... Treatment with metformin can lead to the recovery of pleiotropic biological activities after spinal cord injury.However,its effect on spinal cord injury in aged mice remains unclear.Considering the essential role of angiogenesis during the regeneration process,we hypothesized that metformin activates the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway in endothelial cells,thereby promoting microvascular regeneration in aged mice after spinal cord injury.In this study,we established young and aged mouse models of contusive spinal cord injury using a modified Allen method.We found that aging hindered the recovery of neurological function and the formation of blood vessels in the spinal cord.Treatment with metformin promoted spinal cord microvascular endothelial cell migration and blood vessel formation in vitro.Furthermore,intraperitoneal injection of metformin in an in vivo model promoted endothelial cell proliferation and increased the density of new blood vessels in the spinal cord,thereby improving neurological function.The role of metformin was reversed by compound C,an adenosine monophosphate-activated protein kinase inhibitor,both in vivo and in vitro,suggesting that the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway likely regulates metformin-mediated angiogenesis after spinal cord injury.These findings suggest that metformin promotes vascular regeneration in the injured spinal cord by activating the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway,thereby improving the neurological function of aged mice after spinal cord injury. 展开更多
关键词 adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway ANGIOGENESIS aged mice compound C METFORMIN spinal cord injury
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Fusobacterium nucleatum-induced imbalance in microbiome-derived butyric acid levels promotes the occurrence and development of colorectal cancer 被引量:1
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作者 Qi-Long Wu Xiao-Ting Fang +5 位作者 Xin-Xin Wan Qing-Yong Ding Yan-Jun Zhang Ling Ji Yong-Liang Lou Xiang Li 《World Journal of Gastroenterology》 SCIE CAS 2024年第14期2018-2037,共20页
BACKGROUND Colorectal cancer(CRC)ranks among the most prevalent malignant tumors globally.Recent reports suggest that Fusobacterium nucleatum(F.nucleatum)contributes to the initiation,progression,and prognosis of CRC.... BACKGROUND Colorectal cancer(CRC)ranks among the most prevalent malignant tumors globally.Recent reports suggest that Fusobacterium nucleatum(F.nucleatum)contributes to the initiation,progression,and prognosis of CRC.Butyrate,a short-chain fatty acid derived from the bacterial fermentation of soluble dietary fiber,is known to inhibit various cancers.This study is designed to explore whether F.nucleatum influences the onset and progression of CRC by impacting the intestinal metabolite butyric acid.AIM To investigate the mechanism by which F.nucleatum affects CRC occurrence and development.METHODS Alterations in the gut microbiota of BALB/c mice were observed following the oral administration of F.nucleatum.Additionally,DLD-1 and HCT116 cell lines were exposed to sodium butyrate(NaB)and F.nucleatum in vitro to examine the effects on proliferative proteins and mitochondrial function.RESULTS Our research indicates that the prevalence of F.nucleatum in fecal samples from CRC patients is significantly greater than in healthy counterparts,while the prevalence of butyrate-producing bacteria is notably lower.In mice colonized with F.nucleatum,the population of butyrate-producing bacteria decreased,resulting in altered levels of butyric acid,a key intestinal metabolite of butyrate.Exposure to NaB can impair mitochondrial morphology and diminish mitochondrial membrane potential in DLD-1 and HCT116 CRC cells.Consequently,this leads to modulated production of adenosine triphosphate and reactive oxygen species,thereby inhibiting cancer cell prolif-eration.Additionally,NaB triggers the adenosine monophosphate-activated protein kinase(AMPK)signaling pathway,blocks the cell cycle in HCT116 and DLD-1 cells,and curtails the proliferation of CRC cells.The combined presence of F.nucleatum and NaB attenuated the effects of the latter.By employing small interfering RNA to suppress AMPK,it was demonstrated that AMPK is essential for NaB’s inhibition of CRC cell proliferation.CONCLUSION F.nucleatum can promote cancer progression through its inhibitory effect on butyric acid,via the AMPK signaling pathway. 展开更多
关键词 Colorectal cancer Fusobacterium nucleatum Butyric acid Gut microbiota adenosine monophosphate-activated protein kinase signal pathway
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Antidepressant effect of electroacupuncture regulates signal targeting in the brain and increases brain- derived neurotrophic factor levels 被引量:14
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作者 Dong-mei Duan Ya Tu +1 位作者 Ping Liu Shuang Jiao 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第10期1595-1602,共8页
Electroacupuncture improves depressive behavior faster and with fewer adverse effects than antidepressant medication. However, the antidepressant mechanism of electroacupuncture remains poorly understood. Here, we est... Electroacupuncture improves depressive behavior faster and with fewer adverse effects than antidepressant medication. However, the antidepressant mechanism of electroacupuncture remains poorly understood. Here, we established a rat model of chronic unpredicted mild stress, and then treated these rats with electroacupuncture at Yintang (EX-HN3) and Baihui (DU20) with sparse waves at 2 Hz and 0.6 mA for 30 minutes, once a day. We found increased horizontal and vertical activity, and decreased immobility time, at 2 and 4 weeks after treatment. Moreover, levels of neurotransmitters (5-hydroxytryptamine, glutamate, and y-aminobutyric acid) and protein levels of brain-derived neurotrophic factor and brain-derived neurotrophic factor-related proteins (TrkB, protein kinase A, and phosphorylation of cyclic adenosine monophosphate response element binding protein) were increased in the hippocampus. Similarly, protein kinase A and TrkB mRNA levels were increased, and calcium-calmodulin-dependent protein kinase lI levels decreased. These findings suggest that electroacupuncture increases phosphorylation of cyclic adenosine monophosphate response element binding protein and brain-derived neurotrophic factor levels by regulating multiple targets in the cyclic adenosine rnonophosphate response element binding protein signal- ing pathway, thereby promoting nerve regeneration, and exerting an antidepressive effect. 展开更多
关键词 nerve regeneration depression chronic unexpected mild stress ELECTROACUPUNCTURE brain-derived neurotrophic factor NEUROTRANSMITTER cyclic adenosine monophosphate response element binding protein signal pathway protein kinase A TRKB FLUOXETINE neural regeneration
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Panax quinquefolium saponin Optimizes Energy Homeostasis by Modulating AMPK-Activated Metabolic Pathways in Hypoxia-Reperfusion Induced Cardiomyocytes 被引量:6
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作者 YU Yong-hui ZHANG Pei +3 位作者 WANG Cheng-long LIU Jian-gang LI Peng ZHANG Da-wu 《Chinese Journal of Integrative Medicine》 SCIE CAS CSCD 2021年第8期613-620,共8页
Objective To investigate the effects and underlying mechanisms of Panax quinquefolium saponin(PQS)on energy deficiency in hypoxia-reperfusion(H/R)induced cardiomyocytes.Methods The H/R injury involved hypoxia for 3 h ... Objective To investigate the effects and underlying mechanisms of Panax quinquefolium saponin(PQS)on energy deficiency in hypoxia-reperfusion(H/R)induced cardiomyocytes.Methods The H/R injury involved hypoxia for 3 h and then reperfusion for 2 h.Cardiomyocytes recruited from neonatal rat ventricular myocytes(NRVMs)were randomly divided into control,H/R,H/R+compound C(C.C),H/R+PQS,and H/R+C.C+PQS groups.BrdU assay,lactase dehydrogenase(LDH)leakage and early apoptosis rate were evaluated to assess cell damages.Contents of high energy phosphate compounds were conducted to detect the energy production.Protein expression levels of adenosine monophosphate-activated protein kinase a(AMPKα),glucose transporter 4(GLUT4),phosphate fructose kinase 2(PFK2),fatty acid translocase/cluster of differentiation 36(FAT/CD36),and acetyl CoA carboxylase 2(ACC2)in the regulatory pathways were measured by Western blotting.Immunofluorescence staining of GLUT4 and FAT/CD36 was used to observe the mobilization of metabolic transporters.Results PQS(50 mg/L)pretreatment significantly alleviated H/R-induced inhibition of NRVMs viability,up-regulation of LDH leakage,acceleration of early apoptosis,and reduction of energy production(P<0.05).Compared with the H/R group,up-regulated expression of AMPKα,GLUT4,PFK2,FAT/CD36 and ACC2 were observed,and more GLUT4 and FAT/CD36 expressions were detected on the membrane in the H/R+PQS group(P<0.05).These effects of PQS on H/R-induced NRVMs were eliminated in the H/R+C.C+PQS group(P<0.05).Conclusion PQS has prominent advantages in protecting NRVMs from H/R-induced cell damages and energy metabolic disorders,by activation of AMPKα-mediated GLUT4-PFK2 and FAT/CD36-ACC2 pathways. 展开更多
关键词 Panax quinquefolium saponin Chinese medicine neonatal rat ventricular myocytes hypoxia-reperfusion energy metabolism adenosine monophosphate-activated protein kinaseαpathways
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A pH-responsive polymersome depleting regulatory T cells and blocking A2A receptor for cancer immunotherapy
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作者 Binfen Shao Xuehui Huang +3 位作者 Funeng Xu Jingmei Pan Yi Wang Shaobing Zhou 《Nano Research》 SCIE EI CSCD 2022年第3期2324-2334,共11页
The immunosuppressive tumor microenvironment(ITM)and low immunogenicity of tumors greatly limit cancer immunotherapy efficacy.The approach of solely depleting regulatory T cells(Tregs)cannot ameliorate ITM,but possibl... The immunosuppressive tumor microenvironment(ITM)and low immunogenicity of tumors greatly limit cancer immunotherapy efficacy.The approach of solely depleting regulatory T cells(Tregs)cannot ameliorate ITM,but possibly worsen it since the produced apoptotic Tregs will activate the A2A signaling pathway and cause more severe immune suppression.To address it,in this work a pH-responsive polymersome(CY/ZM@CS-BPA)based on chondroitin sulfate(CS)-poly(β-amino ester)is rationally developed.In the acidic tumor microenvironment,the tertiary amine groups in the polymersome will reverse from hydrophobic to hydrophilic due to protonation,which leads to the disintegration of nanostructures and the release of cyclophosphamide(CY)and A2A receptor(A2AR)antagonist ZM241385(ZM).CY can selectively deplete Tregs.Additionally,CY can induce immunogenic cell death(ICD)of tumor cells,which results in the proapoptotic translocation of calreticulin to the cell surface,further initiating the antitumor immune responses.ZM can inhibit the activation of the adenosine A2A pathway,subsequently preventing the differentiation of CD4^(+)T cells into Tregs and enhancing the cytotoxicity of CD8+T cells.As a result,the combination of depleting regulatory T cells and blocking the A2A receptor can enhance cancer immunotherapy efficacy. 展开更多
关键词 POLYMERSOME regulatory T cells adenosine A2A pathway immunogenic cell death IMMUNOTHERAPY
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