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连翘脂素调节Ras/Raf/MEK/ERK信号通路对结直肠癌细胞恶性生物学行为的影响
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作者 郑声友 李叶若 肖嘉伍 《河北医药》 CAS 2024年第12期1771-1776,共6页
目的 探究连翘脂素(PG)对结直肠癌细胞增殖、迁移、侵袭、凋亡以及上皮间质转化的影响及机制。方法 培养HCT116结直肠癌细胞,采用10~200μmol/L的连翘脂素处理细胞,检测细胞存活率,筛选最佳实验浓度。将细胞分为对照组(Control组),连翘... 目的 探究连翘脂素(PG)对结直肠癌细胞增殖、迁移、侵袭、凋亡以及上皮间质转化的影响及机制。方法 培养HCT116结直肠癌细胞,采用10~200μmol/L的连翘脂素处理细胞,检测细胞存活率,筛选最佳实验浓度。将细胞分为对照组(Control组),连翘脂素低、中、高浓度组(PG-L组、PG-M组、PG-H组),连翘脂素高浓度+转染慢病毒阴性对照组(PG-H+NC组),连翘脂素高浓度+Ras慢病毒组(PG-H+Ras组)。平板克隆形成实验检测细胞增殖;划痕实验检测细胞迁移;Transwell小室法检测细胞侵袭;流式细胞术以及Hoechst33258染色法检测细胞凋亡;Western blot法检测上皮间质转化(EMT)标志蛋白E型钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)以及信号通路相关蛋白p-Raf、p-MEK、p-ERK表达;建立荷瘤小鼠模型评价连翘脂素对结直肠癌肿瘤生长的影响。结果 10~200μmol/L的连翘脂素处理HCT116结直肠癌细胞,可以显著抑制细胞存活率,经计算IC50值为(140.4±2.147)μmol/L,选择10、50、100μmol/L连翘脂素进行后续实验;与Control组比较,PG-L组、PG-M组、PG-H组HCT116细胞克隆形成率、划痕愈合率、细胞侵袭个数以及Vimentin、p-Raf、p-MEK、p-ERK表达显著降低,细胞凋亡率以及E-cadherin表达显著升高,且呈浓度依赖性(P<0.05);与PG-H+NC组比较,PG-H+Ras组HCT116细胞克隆形成率、划痕愈合率、细胞侵袭个数以及Vimentin、p-Raf、p-MEK、p-ERK表达显著升高,细胞凋亡率以及E-cadherin表达显著降低(P<0.05);连翘脂素可以显著抑制结直肠癌移植瘤的生长。结论 连翘脂素可以抑制结直肠癌细胞增殖、迁移、侵袭、凋亡以及上皮间质转化,其作用机制可能与抑制Ras/Raf/MEK/ERK信号通路激活有关。 展开更多
关键词 连翘脂素 ras/raf/MEK/erk信号通路 结直肠癌 上皮间质转化 增殖 凋亡
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Upregulated Ras/Raf/ERK1/2 signaling pathway:a new hope in the repair of spinal cord injury 被引量:6
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作者 Tao Liu Fu-jiang Cao +2 位作者 Dong-dong Xu Yun-qiang Xu Shi-qing Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第5期792-796,共5页
An increasing number of studies report that the Ras/Raf/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway has a death-promoting apoptotic function in neural cells. We hypothesized that the Ras/Raf... An increasing number of studies report that the Ras/Raf/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway has a death-promoting apoptotic function in neural cells. We hypothesized that the Ras/Raf/ERK1/2 signaling pathway may be abnormally regulated in rat injured spinal cord models. The weight drop method was used to establish rat spinal cord injury at T9. Western blot analysis and immunohistochemical staining revealed Ras expression was dramatically elevated, and the phosphorylations of A-Raf, B-Raf and C-Raf were all upregulated in the injured spinal cord. Both mitogen-activated protein kinase kinase 1/2 and ERK1/2, which belong to the Ras/Raf signaling kinases, were upregulated. These results indicate that Ras/Raf/ ERK1/2 signaling may be upregulated in injured spinal cord and are involved in recovery after spinal cord injury. 展开更多
关键词 nerve regeneration ras/raf/erkl/2 signaling pathway spinal cord injury APOPTOSIS REPAIR regulation INHIBITION neural regeneration
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Timosaponin AⅢ induces drug-metabolizing enzymes by activating constitutive androstane receptor (CAR) via dephosphorylation of the EGFR signaling pathway 被引量:1
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作者 Muhammad Zubair Hafiz Jie Pan +4 位作者 Zhiwei Gao Ying Huo Haobin Wang Wei Liu Jian Yang 《Journal of Biomedical Research》 CAS CSCD 2024年第4期382-396,共15页
The current study aimed to assess the effect of timosaponin AⅢ(T-AⅢ)on drug-metabolizing enzymes during anticancer therapy.The in vivo experiments were conducted on nude and ICR mice.Following a 24-day administratio... The current study aimed to assess the effect of timosaponin AⅢ(T-AⅢ)on drug-metabolizing enzymes during anticancer therapy.The in vivo experiments were conducted on nude and ICR mice.Following a 24-day administration of T-AⅢ,the nude mice exhibited an induction of CYP2B10,MDR1,and CYP3A11 expression in the liver tissues.In the ICR mice,the expression levels of CYP2B10 and MDR1 increased after a three-day T-AⅢ administration.The in vitro assessments with HepG2 cells revealed that T-AⅢ induced the expression of CYP2B6,MDR1,and CYP3A4,along with constitutive androstane receptor(CAR)activation.Treatment with CAR siRNA reversed the T-AⅢ-induced increases in CYP2B6 and CYP3A4 expression.Furthermore,other CAR target genes also showed a significant increase in the expression.The up-regulation of murine CAR was observed in the liver tissues of both nude and ICR mice.Subsequent findings demonstrated that T-AⅢ activated CAR by inhibiting ERK1/2 phosphorylation,with this effect being partially reversed by the ERK activator t-BHQ.Inhibition of the ERK1/2 signaling pathway was also observed in vivo.Additionally,T-AⅢ inhibited the phosphorylation of EGFR at Tyr1173 and Tyr845,and suppressed EGF-induced phosphorylation of EGFR,ERK,and CAR.In the nude mice,T-AⅢ also inhibited EGFR phosphorylation.These results collectively indicate that T-AⅢ is a novel CAR activator through inhibition of the EGFR pathway. 展开更多
关键词 timosaponin AⅢ CAR metabolism enzyme erk1/2 signaling pathway EGFR signaling pathway
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Longan Aril Reverses H2O2 Cytotoxicity in PC12 Cells via RAS/MEK/ERK Signaling Pathway
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作者 Tianrong LEI Yang CAO +4 位作者 Chang LI Jianghua ZHANG Honghe XIAO Cheng SONG Hongyan LI 《Medicinal Plant》 CAS 2021年第2期54-59,共6页
[Objectives]To explore the neuroprotective effects and mechanism of Longan Aril(LA)effective parts on PC12 cells injured by H2O2.[Methods]The neuroprotective effects of LA were evaluated by the cell viability,SOD and ... [Objectives]To explore the neuroprotective effects and mechanism of Longan Aril(LA)effective parts on PC12 cells injured by H2O2.[Methods]The neuroprotective effects of LA were evaluated by the cell viability,SOD and MDA content,apoptosis assay and relative protein expression of Aβand p-Tau.The neuroprotective mechanism of LA was studied by using metabolomics and network pharmacology,and the expressions of RAS/MEK/ERK signaling pathway-related proteins were detected by western blotting.[Results]LA could improve the cell survival rate and SOD content,and reduce apoptosis and expression of Aβand p-tau.Inhibition of RAS/MEK/ERK signaling pathway is a possible mechanism of LA neuroprotective effects.[Conclusions]LA has a neuroprotective effects in vitro and be likely to inhibit the process of AD by inhibition of RAS/MEK/ERK signalling pathway. 展开更多
关键词 Longan Aril(LA) ras/MEK/erk pathway Alzheimer's disease(AD) Neuroprotective effects
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Ras信号通路参与调控细胞凋亡作用的研究进展 被引量:1
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作者 范苏苏 罗兴炜 +1 位作者 朱钰珊(综述) 张旋(审校) 《医学研究与战创伤救治》 CAS 北大核心 2024年第2期191-196,共6页
细胞凋亡是由体内和体外因素触发的预先存在的细胞死亡过程引起的主动细胞死亡,通过清除老化、受损细胞来维持内部环境的稳定。细胞凋亡在生理和病理状态下均发挥重要作用,并受到细胞内多条信号通路的调节,影响细胞内物质的表达。目前已... 细胞凋亡是由体内和体外因素触发的预先存在的细胞死亡过程引起的主动细胞死亡,通过清除老化、受损细胞来维持内部环境的稳定。细胞凋亡在生理和病理状态下均发挥重要作用,并受到细胞内多条信号通路的调节,影响细胞内物质的表达。目前已知Ras信号通路不仅广泛参与调控细胞生长增殖、分化和凋亡等多个生理病理过程,并具有促进细胞发生自噬性死亡的作用,然而,其参与调节细胞凋亡的具体机制尚未完全阐明。文章从细胞凋亡的分子机制出发,重点从线粒体凋亡途径、死亡受体凋亡途径、内质网应激凋亡途径相关凋亡途径,以及Ras信号通路在细胞凋亡调控中的研究进展进行综述。 展开更多
关键词 ras/raf/MEK/erk信号通路 ras/PI3K/Akt信号通路 细胞凋亡
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Acupuncture at Back-Shu point improves insomnia by reducing inflammation and inhibiting the ERK/NF-κB signaling pathway 被引量:1
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作者 Ming-Ming Zhang Jing-Wei Zhao +2 位作者 Zhi-Qiang Li Jing Shao Xi-Yan Gao 《World Journal of Psychiatry》 SCIE 2023年第6期340-350,共11页
BACKGROUND Insomnia is a disease where individuals cannot maintain a steady and stable sleep state or fail to fall asleep.Western medicine mainly uses sedatives and hypnotic drugs to treat insomnia,and long-term use i... BACKGROUND Insomnia is a disease where individuals cannot maintain a steady and stable sleep state or fail to fall asleep.Western medicine mainly uses sedatives and hypnotic drugs to treat insomnia,and long-term use is prone to drug resistance and other adverse reactions.Acupuncture has a good curative effect and unique advantages in the treatment of insomnia.AIM To explore the molecular mechanism of acupuncture at Back-Shu point for the treatment of insomnia.METHODS We first prepared a rat model of insomnia,and then carried out acupuncture for 7 consecutive days.After treatment,the sleep time and general behavior of the rats were determined.The Morris water maze test was used to assess the learning ability and spatial memory ability of the rats.The expression levels of inflammatory cytokines in serum and the hippocampus were detected by ELISA.qRTPCR was used to detect the mRNA expression changes in the ERK/NF-κB signaling pathway.Western blot and immunohistochemistry were carried out to evaluate the protein expression levels of RAF-1,MEK-2,ERK1/2 and NF-κB.RESULTS Acupuncture can prolong sleep duration,and improve mental state,activity,diet volume,learning ability and spatial memory.In addition,acupuncture increased the release of 1L-1β,1L-6 and TNF-αin serum and the hippocampus and inhibited the mRNA and protein expression of the ERK/NF-κB signaling pathway.CONCLUSION These findings suggest that acupuncture at Back-Shu point can inhibit the ERK/NF-κB signaling pathway and treat insomnia by increasing the release of inflammatory cytokines in the hippocampus. 展开更多
关键词 erk/NF-κB signaling pathway ACUPUNCTURE INSOMNIA INFLAMMATION Acupuncture at Back-Shu point Traditional Chinese medicine
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mTOR抑制剂联合熊去氧胆酸对肝癌大鼠抑制、免疫逃逸及Ras/ERK信号通路的影响
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作者 杨雅萌 罗丹凤 《肝脏》 2023年第7期789-793,共5页
目的探究mTOR抑制剂联合熊去氧胆酸(UDCA)对肝癌大鼠抑制、免疫逃逸及Ras/ERK信号通路的影响。方法SPF级SD雄性大鼠60只,10只作为正常(NO)组,50只腹腔注射二乙基亚硝铵进行肝癌建模。建模成功后,取40只大鼠随机分为模型(MO)组,mTOR抑制... 目的探究mTOR抑制剂联合熊去氧胆酸(UDCA)对肝癌大鼠抑制、免疫逃逸及Ras/ERK信号通路的影响。方法SPF级SD雄性大鼠60只,10只作为正常(NO)组,50只腹腔注射二乙基亚硝铵进行肝癌建模。建模成功后,取40只大鼠随机分为模型(MO)组,mTOR抑制剂(MI)组,UDCA(UD)组,mTOR抑制剂联合UDCA(UN)组,每组10只。MI组灌胃mTOR抑制剂西罗莫司2 mg/kg,UD组灌胃UDCA 30 mg/kg,UN组灌胃mTOR抑制剂西罗莫司2 mg/kg及30 mg/kg UDCA,NO组、MO组灌胃同体积0.9%NaCl溶液。观察大鼠肿瘤生长情况、肝组织病理形态,ELISA法检测免疫逃逸相关因子,免疫印迹法检测Ras/ERK信号通路相关蛋白表达。结果与NO组相比,MO组体重显著降低(P<0.05),肝重、肝脏系数显著升高(P<0.05);与MO组相比,MI组体重明显升高(P<0.05),肝重、肝脏系数显著降低(P<0.05);与MI组相比,UD组体重、肝重、肝脏系数无明显差异(P>0.05);与UD组相比,UN组体重明显升高(P<0.05),肝重、肝脏系数显著降低(P<0.05)。与MO组相比,MI组抑瘤曲线明显升高(P<0.05);与MI组相比,UD组抑瘤曲线无明显差异(P>0.05);与UD组相比,UN组抑瘤曲线明显升高(P<0.05)。NO组肝组织及肝小叶结构清晰完整,肝细胞分界清晰且呈放射状排列,未见增生坏死细胞及炎性细胞,MO组肝组织肝索结构不清,肝细胞排列紊乱且细胞肿胀,可见癌巢及大量炎性细胞浸润。与MO组比较,MI组、UD组、UN组病理结构明显改善,炎性细胞及癌细胞明减少。与NO组比较,MO组大鼠血清IL-4、IL-10、TGF-β1含量显著升高(P<0.05);与MO组比较,MI组、UD组、UN组大鼠血清IL-4、IL-10、TGF-β1含量显著降低(P<0.05),且UD组与MI组相比基本无差异(P>0.05),UN组比UD组降低显著(P<0.05)。NO组、MO组、MI组、UD组、UN组Ras蛋白表达分别为1.16±0.11、2.26±0.29、1.51±0.17、1.55±0.18、1.19±0.14,p-ERK蛋白表达分别为1.05±0.10、2.94±0.28、1.66±0.14、1.68±0.16、1.14±0.11;与NO组比较,MO组大鼠肝组织Ras、p-ERK蛋白表达显著升高(P<0.05);与MO组比较,MI组、UD组、UN组大鼠肝组织Ras、p-ERK蛋白表达显著降低(P<0.05),且UD组与MI组相比基本无差异(P>0.05),UN组比UD组降低显著(P<0.05)。结论mTOR抑制剂联合UDCA可显著抑制肝癌大鼠肿瘤生长,抑制免疫逃逸及Ras/ERK信号通路激活。 展开更多
关键词 MTOR抑制剂 熊去氧胆酸(UDCA) 肝癌 免疫逃逸 ras/erk信号通路
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MEK/ERK signaling pathway in apoptosis of SW620 cell line and inhibition effect of resveratrol 被引量:4
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作者 Hao Chen Zhi-Liang Jin Hai Xu 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2016年第1期46-50,共5页
Objective:To study the involvement of MAPK MEK/ERK signaling transduction pathway in the apoptosis process of SW620 tumor cell line and the inhibition effect of resveratrol.Methods:SW620 cell lines were divided into 5... Objective:To study the involvement of MAPK MEK/ERK signaling transduction pathway in the apoptosis process of SW620 tumor cell line and the inhibition effect of resveratrol.Methods:SW620 cell lines were divided into 5 groups,namely,control group.PD98059 group,low-dose resveratrol group,mid-dose resveratrol group and high-dose resveratrol group.The inhibition rate of cell proliferation was detected by MTT method.The expression of apoptotic molecules and MEK/ERK signaling pathway related proteins were assayed by realtime PCR and Western blotting.Results:Compared with control group,the proliferation of cells treated with resveratrol was significantly inhibited.In the case of apoptotic molecules,the expression of Bax,Caspase 3 and Caspase 9 was increased significantly while the expression of anti-apoptotic molecule Bcl2 was decreased significantly in resveratrol groups with a dosedependent manner.In the case of molecules in MEK/ERK signaling pathway,the expression of Ras,Raf,MEK and ERKl/2 was decreased significantly in resveratrol groups with a dose-dependent manner.Conclusions:PD98059 and resveratrol can effectively inhibit the proliferation of SW620 through inhibiting the MEK/ERK signaling pathway. 展开更多
关键词 COLON cancer APOPTOSIS MEK/erk signaling pathway RESVEraTROL Inhibition of proliferation
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枳葛口服液通过Syk/Ras/ERK信号通路防治酒精性肝损伤机制研究
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作者 苟沙沙 黄晓平 +3 位作者 李波 王晓栋 黄素琼 魏嵋 《中医药临床杂志》 2023年第8期1560-1565,共6页
目的:基于Syk/Ras/ERK信号通路观察枳葛口服液含药血清对酒精性肝损伤大鼠BRL3A肝细胞炎症反应的影响,探讨枳葛口服液防治酒精性肝损伤的相关机制。方法:将正常大鼠BRL3A肝细胞接种于6孔板,贴壁后分为正常对照组、模型组(2.5%乙醇处理)... 目的:基于Syk/Ras/ERK信号通路观察枳葛口服液含药血清对酒精性肝损伤大鼠BRL3A肝细胞炎症反应的影响,探讨枳葛口服液防治酒精性肝损伤的相关机制。方法:将正常大鼠BRL3A肝细胞接种于6孔板,贴壁后分为正常对照组、模型组(2.5%乙醇处理)、阳性对照组(美他多辛含药血清加2.5%乙醇)和不同浓度枳葛口服液含药血清(2.5%、5%、10%枳葛口服液含药血清加2.5%乙醇)干预组,24h后酶标法检测各组细胞上清液中GGT(γ-谷氨酰转肽酶)、LDH(乳酸脱氢酶)含量;RT-PCR法测定各组细胞内Syk、Ras、MEK1/2、ERK1/2、c-Fos mRNA表达情况。结果:与正常对照组比较,模型组细胞上清液中GGT、LDH含量显著升高(P<0.01);Syk、Ras、MEK1/2、ERK1/2、c-Fos mRNA表达显著升高(P<0.01)。与模型组比较,各干预组以上指标均呈现不同程度的好转,其中10%枳葛口服液含药血清及阳性对照组作用最显著(P<0.01),二者之间未见明显差异(P>0.05)。结论:一定浓度的枳葛口服液含药血清对大鼠肝细胞酒精性肝损伤具有防治作用,其机制可能与抑制Syk/Ras/ERK信号通路活化,从而减轻肝脏炎症相关。 展开更多
关键词 枳葛口服液 Syk/ras/erk信号通路 酒精性肝损伤 炎症反应
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Yi Qi Jie Du Formula and Salinomycin Combination Treatment Mediates Nasopharyngeal Carcinoma Stem Cell Proliferation,Migration and Apoptosis via CD44/Ras Signaling Pathway 被引量:7
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作者 HE Lan ZHOU Fang-Liang +5 位作者 ZOU Pan WANG Xian-Wen JIANG Yi-Lan HE Ying-Chun LIAO Duan-Fang CAO De-Liang 《Digital Chinese Medicine》 2020年第4期297-308,共12页
Objective To assess the effects of Yi Qi Jie Du Formula(YQJDF)combined with salinomycin(SAL)on nasopharyngeal carcinoma stem cells(NPC-SCs)and investigate the underlying molecular mechanisms.Methods Cell counting meth... Objective To assess the effects of Yi Qi Jie Du Formula(YQJDF)combined with salinomycin(SAL)on nasopharyngeal carcinoma stem cells(NPC-SCs)and investigate the underlying molecular mechanisms.Methods Cell counting methods,the CCK-8 assay,transwell migration assay and JC-1 staining,were used to observe the effects of the combination on the proliferation,migration and apoptosis of NPC stem cells,respectively.Western blot was used to detect the levels of protein in NPC-SCs.Results YQJDF combined with SAL had a synergistic effect on the inhibition of proliferation and migration and induction of NPCSC apoptosis.Mechanistically,YQJDF combined with SAL synergistically upregulated the levels of apoptotic proteins,including cleaved Caspase-3,cleaved Caspase-7 and cleaved Caspase-9.Moreover,YQJDF combined with SAL synergistically decreased the levels of CD44,p-c-Src,Ras,p-PKCδ,p-MEK,p-c-Raf,p-ERK1/2 and p-AKT proteins.Conclusions The combination of YQJDF and SAL has a synergistic effect on the inhibition of NPC-SC proliferation and migration and induction of apoptosis,which may be closely related to the downregulation of the CD44/Ras signaling pathway. 展开更多
关键词 Yi Qi Jie Du Formula(YQJDF) SALINOMYCIN Nasopharyngeal carcinoma stem cells (NPC-SCs) PROLIFEraTION Apoptosis CD44/ras signaling pathway
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The role of ERK1/2 signaling pathway in coronary microembolization-induced rat myocardial inflammation and injury 被引量:1
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作者 LI Lang,LI Dong-hua,QU Nan,WEN Wei-ming,HUANG Wei-qiang (Department of Cardiology,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China) 《岭南心血管病杂志》 2011年第S1期190-190,共1页
Objectives In this work,we explore the effect of atorvastatin on myocardial apoptosis and caspase-8 acti- vation after coronary microembolization(CME) in rats. Methods Fifty rats were randomly divided into five groups... Objectives In this work,we explore the effect of atorvastatin on myocardial apoptosis and caspase-8 acti- vation after coronary microembolization(CME) in rats. Methods Fifty rats were randomly divided into five groups; the coronary microembolization(CME) group,the sham-operated (sham) control group,the gastric lavage control group, the atorvastatin lavage group,and the caspasse-8 inhibitor (N-acetyl-Ile-Glu-Thr-Asp-CHO,abbreviated as CHO) group,with 10 rats for each group.A microembolization ball was injected through the left ventricle for constructing the CME model.Animals in the sham control group were given an injection of physiological saline instead of the microembolization ball.Seven days before the operation,the atorvastatin group underwent gastric lavage with 20 mg/kg of atorvastatin once a day.Gastric lavage control animals underwent gastric lavage with an equivalent dose of physiological saline instead of the atorvastatin.Animals in the CHO group were given an intraperitoneal injection of 10 mg/kg of CHO 30 min before the operation.Six hours after the operation,cardiac ultrasonic detection was conducted on each group to measure the cardiac function indexes.TUNEL(Terminal-deoxynucleoitidyl transferase mediated dUTP nick end labeling) assays were used to measure myocardial apoptosis,and western blots were used to quantify the expression levels of activated caspase-3 and -8.Results(1) The echocardiographic parameters showed that,compared to the sham control animals,the left ventricular ejection fraction(LVEF) of the CME group was significantly decreased(P【0.05).In addition, cardiac sonography revealed a decrease in the left ventricular shortening fraction(FS) and cardiac output(CO), but an increase in the left ventricular end-diastolic dimension (LVEDd).Compared to the CME group,the atorvastatin and CHO groups exhibited significantly improved cardiac function (P【0.05).(2) When compared with the sham control,the myocardical apoptotic rate of the CME group,as well as the levels of activated caspase-3 and-8,increased significantly (P【0.05).The myocardial apoptotic rate,as well as the levels of activated caspase-3 and caspase-8 in the atorvastatin and CHO groups,decreased significandy(P【0.05) in comparison to the CME group.Conclusions The atorvastatin pretreatment clearly suppressed post-CME myocardial apoptosis and improved cardiac function.The most likely mechanism for these effects is the blockade of the myocardial death receptor -mediated apoptosis pathway. 展开更多
关键词 erk The role of erk1/2 signaling pathway in coronary microembolization-induced rat myocardial inflammation and injury
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Maleylated-BSA induces TNF-α production through the ERK and NF-κB signaling pathways in murine RAW264.7 macrophages
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作者 Rui Tada Yusuke Koide +4 位作者 Mitsuaki Yamamuro Akira Hidaka Koichiro Nagao Yoichi Negishi Yukihiko Aramaki 《Open Journal of Immunology》 2013年第4期184-189,共6页
Ligands for macrophage scavenger receptors are reported to induce a wide range of host cell responses, including the production of inflammatory cytokines;however, the underlying mechanisms have not yet been fully unde... Ligands for macrophage scavenger receptors are reported to induce a wide range of host cell responses, including the production of inflammatory cytokines;however, the underlying mechanisms have not yet been fully understood and which remain obscure. In this study, we have examined the effect of maleylated bovine serum albumin (maleylated-BSA), a well-known ligand of the scavenger receptor, on the murine macrophage cell line RAW264.7. Maleylated-BSA strongly induced the production of tumor necrosis factor-α (TNF-α) and induced phosphorylation of extracellular signal-regulated kinase (ERK) and NF-kB p65. We also observed that maleylated-BSA-induced TNF-α production was blocked by the ERK inhibitor U0126. Together, these data demonstrates that maleylated-BSA- induced production of TNF-α requires the ERK/NF-κB signaling cascade in murine RAW- 264.7 macrophages. 展开更多
关键词 Maleylated-BSA erk MACROPHAGES signaling pathway TNF-Α
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VEGFR2 mediated RAS/MAPK signaling pathway to explore the mechanism of Bushen Antai Granule in the treatment of recurrent abortion
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作者 Wei Chang Wei-Li Li Sha-Sha Lu 《Journal of Hainan Medical University》 2021年第9期30-36,共7页
Objective:To investigate the effect of Bushen Antai Granule on the mRNA and protein expression of Ras protein/mitogen activated protein kinase mediated by vascular endothelial growth factor receptor 2 with small inter... Objective:To investigate the effect of Bushen Antai Granule on the mRNA and protein expression of Ras protein/mitogen activated protein kinase mediated by vascular endothelial growth factor receptor 2 with small interference RNA interference.Methods:Method to construct the placenta microvascular endothelial cells,and the preparation of kidney fetus granule drug-containing serum,select the best drug-containing serum concentration,it can be divided into normal group,the serum siRNA-NC normal serum group,drug serum,siRNA normal serum group,siRNA drug serum group,using real-time fluorescent quantitative PCR,Western blotting,immunofluorescence test respectively the RAS/MAPK mRNA and protein expression.Results:Results there was no significant difference in Ras and MAPK mRNA and protein expression between the normal group and the negative control group(P>0.05).The mRNA and protein expressions of Ras and MAPK in the drug serum group were significantly higher than those in the normal serum group(P<0.01).Ras and MAPK mRNA and protein expression were significantly decreased in siRNA1 normal serum group compared with normal serum group(P<0.01).Ras,MAPK mRNA and protein expression in siRNA1 drug serum group were significantly different from that in siRNA1 normal serum group(P<0.01).Conclusion:Conclusion The therapeutic effect of Bushen Antai Granule on recurrent abortion may be realized by upregulation of RAS/MAPK mRNA and protein expression. 展开更多
关键词 Bushen Antai Granule Recurrent spontaneous abortion Placental microvascular endothelial cells Drug-containing serum ras/MAPK signaling pathway
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吉祥草中甾体皂苷RCE-4对人宫颈癌Caski细胞Ras/Erk和p16/cyclinD1/CDK4通路的影响 被引量:6
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作者 颜为红 邹坤 +6 位作者 贺海波 张永峰 李小妹 李小琴 杨小姣 汪鋆植 邓张双 《中国临床药理学与治疗学》 CAS CSCD 2018年第3期247-254,共8页
目的:研究吉祥草中甾体皂苷RCE-4影响Ras/Erk和p16/cyclin D1/CDK4信号通路促进Caski细胞凋亡的作用机制。方法:体外培养人宫颈癌Caski细胞株,用RCE-4作为处理因素,MTT法检测细胞增殖活力;流式细胞术检测细胞周期分布;Real-time PCR检测... 目的:研究吉祥草中甾体皂苷RCE-4影响Ras/Erk和p16/cyclin D1/CDK4信号通路促进Caski细胞凋亡的作用机制。方法:体外培养人宫颈癌Caski细胞株,用RCE-4作为处理因素,MTT法检测细胞增殖活力;流式细胞术检测细胞周期分布;Real-time PCR检测p16、cyclin D1和CDK4m RNA表达水平;Western blot检测Ras/Erk信号通路总蛋白和磷酸化蛋白表达水平。结果:RCE-4呈剂量依赖性抑制Caski细胞增殖,其作用24 h的IC50值为12.33μmol/L;升高G0/G1期细胞比例,降低S期细胞比例;抑制Ras、p-Raf、p-Mek1/2和p-Erk1/2蛋白表达,降低p-Raf/Raf、p-Mek1/2/Mek1/2和p-Erk1/2/Erk1/2比值,上调p16的m RNA表达,下调cyclin D1和CDK4的m RNA表达。结论:RCE-4可抑制Caski细胞的增殖,诱导细胞在G0/G1期阻滞,其诱导作用与其抑制Ras/Erk和p16/cyclin D1/CDK4信号通路激活有关。 展开更多
关键词 RCE-4 细胞周期 CASKI细胞 ras/erk信号通路 p16/cyclinD1/CDK4信号通路
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新藤黄酸通过Ras/Raf/Erk信号通路诱导肺腺癌A549细胞凋亡的研究 被引量:8
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作者 彭程 孙美灵 +1 位作者 苏婧婧 李庆林 《中药新药与临床药理》 CAS CSCD 北大核心 2016年第2期189-193,共5页
目的研究新藤黄酸(Gambogenic acid,GNA)诱导A549细胞凋亡的作用,并探讨其可能的分子机制。方法采用噻唑蓝(MTT)法检测0.5,1.0,2.0,4.0,8.0μmol·L^(-1)的GNA作用于A549细胞24 h后细胞的增殖情况;采用Hoechst 33342和Annexin V-FIT... 目的研究新藤黄酸(Gambogenic acid,GNA)诱导A549细胞凋亡的作用,并探讨其可能的分子机制。方法采用噻唑蓝(MTT)法检测0.5,1.0,2.0,4.0,8.0μmol·L^(-1)的GNA作用于A549细胞24 h后细胞的增殖情况;采用Hoechst 33342和Annexin V-FITC/PI染色法,于荧光显微镜下观察1.25,2.5,5.0μmol·L^(-1)的GNA作用细胞24 h后的凋亡形态;流式细胞仪检测1.25,2.5,5.0μmol·L^(-1)的GNA作用细胞24 h后的凋亡率;Western Blot法检测1.25,2.5,5.0μmol·L^(-1)的GNA处理细胞24 h后,Ras、Raf、Erk和p-Erk的表达。结果GNA能够显著降低A549细胞的活力,并呈浓度依赖性抑制细胞增殖,24 h的IC50为2.507μmol·L^(-1);Hoechst33342和AV/PI染色后,于荧光显微镜下观察发现,细胞显示明显的凋亡特征;流式细胞仪检测结果表明,随着GNA浓度的升高,细胞的凋亡比率逐渐上升;Western Blot法检测显示GNA能够抑制Ras、Raf、p-Erk1/2蛋白的表达。结论 GNA能够诱导A549细胞凋亡,其作用可能与通过调控Ras/Raf/Erk信号通路有关。 展开更多
关键词 新藤黄酸 A549细胞 凋亡 ras/raf/erk信号通路 肺癌
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抗纤抑癌方对肝癌前病变大鼠Ras/Erk信号通路的调控作用研究 被引量:3
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作者 杨先照 刘蕊洁 +3 位作者 焦云涛 张鹏 李莹 叶永安 《世界中西医结合杂志》 2018年第10期1340-1343,共4页
目的观察抗纤抑癌方对肝癌前病变大鼠Ras/Erk信号通路的调控作用,探讨抗纤抑癌方防治肝癌前病变的作用机制。方法雄性Wistar大鼠55只,随机分为正常组10只,模型组、扶正化瘀组及抗纤抑癌组各15只。模型组、扶正化瘀组及抗纤抑癌组均以二... 目的观察抗纤抑癌方对肝癌前病变大鼠Ras/Erk信号通路的调控作用,探讨抗纤抑癌方防治肝癌前病变的作用机制。方法雄性Wistar大鼠55只,随机分为正常组10只,模型组、扶正化瘀组及抗纤抑癌组各15只。模型组、扶正化瘀组及抗纤抑癌组均以二乙基亚硝胺(50 mg/kg)腹腔注射诱导肝癌前病变形成,每周1次,持续14周。正常组予生理盐水腹腔注射作为对照。同时,连续给予相应药物灌胃干预,1次/d,在第14周末取材。采用HE和Masson染色以观察大鼠肝癌前病变情况及纤维化程度;采用Western-Blot方法检测大鼠肝脏中Ras、Erk及p-Erk蛋白的表达情况。结果 HE和Masson染色显示模型组肝脏细胞异常增生明显,纤维化程度较重。与模型组比较,抗纤抑癌组和扶正化瘀组肝脏纤维堆积及肝细胞异常增生情况明显减轻,尤其以抗纤抑癌组作用明显。Western-Blot结果显示,p-Erk在模型组中高表达,与正常组比较,两者之间差异有统计学意义(P <0. 05);抗纤抑癌组p-Erk表达低于模型组、扶正化瘀组,分别与之比较,差异均具有统计学意义(P <0. 05);扶正化瘀组与模型组之间比较差异无统计学意义(P> 0. 05)。Erk表达在各组间差异无统计学意义(P> 0. 05)。Erk磷酸化率(p-Erk/Erk)在模型组中最高,与正常组比较,两者之间差异有统计学意义(P <0. 05);抗纤抑癌组p-Erk/Erk低于模型组、扶正化瘀组,分别与之比较,差异均具有统计学意义(P <0. 05);扶正化瘀组与模型组之间差异比较无统计学意义(P> 0. 05)。Ras表达在各组间比较差异无统计学意义(P> 0. 05)。结论抗纤抑癌方具有抗纤维化、阻断肝癌前病变的作用,并能抑制肝癌前病变大鼠Ras/Erk信号通路的激活,这可能是其防治肝癌前病变的作用机制之一。 展开更多
关键词 抗纤抑癌方 肝癌前病变 ras/erk信号通路
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大鼠增殖抑制基因通过Ras-Raf-MEK-ERK信号通路抑制C6胶质瘤细胞增殖 被引量:2
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作者 蒋树财 邹有瑞 +5 位作者 高鹏 郭晖 霍国进 王军成 赵巍 沈冰 《中风与神经疾病杂志》 CAS 北大核心 2015年第10期884-888,共5页
目的探讨Ras-Raf-MEK-ERK通路在大鼠增殖抑制基因(r HSG)抑制C6大鼠胶质瘤细胞增殖中的作用。方法用r HSG过表达腺病毒载体(Adv-r HSG-GFP)转染C6细胞后,流式细胞仪分析腺病毒转染效率;Western blot检测r HSG蛋白表达变化;流式细胞仪分... 目的探讨Ras-Raf-MEK-ERK通路在大鼠增殖抑制基因(r HSG)抑制C6大鼠胶质瘤细胞增殖中的作用。方法用r HSG过表达腺病毒载体(Adv-r HSG-GFP)转染C6细胞后,流式细胞仪分析腺病毒转染效率;Western blot检测r HSG蛋白表达变化;流式细胞仪分析细胞周期;qRT-PCR检测H-ras、N-ras、K-ras、Erk1、Erk2基因mRNA表达变化;Western blot检测H-ras、N-ras、K-ras、p-Erk1/2、Erk1/2、p-Rb、Rb蛋白表达变化。结果腺病毒载体能高效的转染C6细胞并表达GFP蛋白,Adv-r HSG-GFP组r HSG蛋白表达显著高于未转染组(PBS)和AdvGFP组,C6细胞被阻滞于G0/G1期(P<0.01);经IGF-1刺激后,Adv-r HSG-GFP组细胞H-ras、N-ras、K-ras、Erk1、Erk2基因的mRNA和蛋白表达水平与PBS组和Adv-GFP组无明显差异(P>0.05);Adv-r HSG-GFP组细胞过表达r HSG能显著抑制IGF-1诱导的Erk1/2的活化,p-Erk1/2蛋白表达量显著低于其余两组(P<0.01);同时其p-Rb蛋白的表达量显著低于其余两组(P<0.01),而Rb蛋白表达量3组无明显差异(P>0.05)。结论 r HSG可能通过抑制Ras-Raf-MEK-ERK信号通路的激活抗C6恶性胶质瘤细胞增殖。 展开更多
关键词 大鼠增殖抑制基因 rHSG ras-raf-MEK-erk信号通路 ras erk1/2 胶质瘤
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基于Ras/Raf-1/ERK信号转导通路调控VEGF的表达探讨活血解毒方对糖尿病大鼠视网膜的影响 被引量:7
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作者 郝改梅 何洁 +6 位作者 韩静 吴晏 武志黔 袁悦莹 毛颖秋 王伟 毕力夫 《世界中医药》 CAS 2015年第5期757-761,共5页
目的:观察活血解毒方对糖尿病大鼠视网膜血管形态的影响并探讨其可能的作用机制。方法:一次性腹腔注射链脲佐菌素(Streptozotocin,STZ,65 mg/kg)诱导糖尿病大鼠模型,造模后随机分为模型组和活血解毒方组。另设正常对照组。药物干预12周... 目的:观察活血解毒方对糖尿病大鼠视网膜血管形态的影响并探讨其可能的作用机制。方法:一次性腹腔注射链脲佐菌素(Streptozotocin,STZ,65 mg/kg)诱导糖尿病大鼠模型,造模后随机分为模型组和活血解毒方组。另设正常对照组。药物干预12周后,应用视网膜消化铺片法观察视网膜血管形态;应用Western blot法检测视网膜VEGF蛋白的表达,应用Real-Time PCR法检测视网膜VEGF、Ras、Raf-1与ERK mRNA的表达。结果:模型组视网膜毛细血管面积密度及内皮细胞/周细胞比例与较正常组升高(P<0.001),VEGF蛋白及VEGF、Ras、ERKmRNA表达升高(P<0.05),Raf-1mRNA表达升高(P>0.05)。与模型组比较,活血解毒方组视网膜毛细血管面积密度和内皮细胞/周细胞比例降低(P<0.01和P<0.001),VEGF蛋白与VEGF、Ras、Raf-1、ERK mRNA表达下降(P<0.05)。结论:活血解毒方能明显抑制视网膜毛细血管和内皮细胞的增生,其机制可能是通过干预Ras/Raf-1/ERK信号转导通路,下调VEGF在视网膜中的表达,抑制血管新生,从而改善DR。 展开更多
关键词 糖尿病视网膜病变 活血解毒方 血管内皮生长因子 ras/raf-1/erk信号转导通路
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ERK1/2信号通路阻断剂PD98059对慢性高原病患者骨髓有核红细胞中Ras、BRaf、MEK、ERK1/2表达的影响 被引量:4
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作者 韩园芳 冀林华 +3 位作者 冯婷婷 刘芳 崔森 苏娟 《中国实验血液学杂志》 CAS CSCD 北大核心 2017年第5期1571-1575,共5页
目的:探讨ERK1/2信号通路阻断剂PD98059对Ras、B型丝/苏氨酸蛋白激酶(BRaf)、丝裂原活化蛋白激酶(MEK)、细胞信号调节激酶1/2(ERK1/2)表达的影响,以期为慢性高原病(chronic mountain sickness,CMS)的基础研究和临床治疗探讨新的途径。方... 目的:探讨ERK1/2信号通路阻断剂PD98059对Ras、B型丝/苏氨酸蛋白激酶(BRaf)、丝裂原活化蛋白激酶(MEK)、细胞信号调节激酶1/2(ERK1/2)表达的影响,以期为慢性高原病(chronic mountain sickness,CMS)的基础研究和临床治疗探讨新的途径。方法:选取CMS患者16例,取骨髓液分离单个核细胞,以CD71与CD235a抗体磁珠分选阳性细胞,将细胞分为5组:空白对照组、DMSO溶剂组及PD98059 5、10和20μmol/L组。在低氧条件下培养72 h,应用ELISA法测定培养骨髓有核红细胞上清液中Ras-GTP水平,RT-PCR法测定骨髓有核红细胞中BRaf、MEK、ERK1/2 mRNA的表达,Western blot方法检测骨髓有核红细胞中p-BRaf、p-MEK、pERK1/2蛋白表达。结果:PD98059对各组Ras-GTP的水平无明显影响(P=0.798)。溶剂组与空白对照组相比,BRaf、MEK mRNA的表达水平差异无统计学意义(P=0.826、P=0.298)。与PD98059 20 mol/L比较,其余4组ERK1/2 mRNA的表达水平差异有统计学意义(P=0.001、P=0.002)。溶剂组与空白对照组相比,p-BRaf、p-MEK蛋白的表达差异无统计学意义(P=0.370、P=0.351)。与PD98059 20 mol/L比较,其余4组p-ERK1/2蛋白水平差异有统计学意义(P<0.001、P<0.007)。结论:PD98059能下调骨髓有核红细胞ERK1/2 mRNA及p-ERK1/2蛋白的表达。Ras/Raf/MEK/ERK 1/2通路是调控CMS骨髓有核红细胞的主要信号传导途径,可能参与了慢性高原病的发病过程。 展开更多
关键词 慢性高原病 erk1/2信号通路 PD98059 骨髓有核红细胞 ras BraF MEK erk1/2
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基于Ras/ERK信号通路益肾通癃汤对人前列腺癌PC-3细胞增殖、凋亡、侵袭及迁移的影响 被引量:2
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作者 刘德果 李姿蓉 +5 位作者 陈其华 赵姣 杨磊 李博 向时竹 林梦姣 《中国中医药信息杂志》 CAS CSCD 2021年第7期60-65,共6页
目的观察益肾通癃汤对人前列腺癌PC-3细胞增殖、凋亡、侵袭及迁移能力的影响,从Ras/ERK信号通路调控角度初步探讨其作用机制。方法将PC-3细胞分为空白血清组和益肾通癃汤药物血清高、中、低剂量组(益肾通癃汤高、中、低剂量组),CCK-8法... 目的观察益肾通癃汤对人前列腺癌PC-3细胞增殖、凋亡、侵袭及迁移能力的影响,从Ras/ERK信号通路调控角度初步探讨其作用机制。方法将PC-3细胞分为空白血清组和益肾通癃汤药物血清高、中、低剂量组(益肾通癃汤高、中、低剂量组),CCK-8法观察PC-3细胞增殖,倒置显微镜下观察细胞形态;Annexin V-FITC/PI双染色法检测细胞凋亡,Transwell小室检测PC-3细胞侵袭及迁移能力,Western blot检测PC-3细胞Ras/ERK信号通路相关蛋白及锌指转录因子(Snail)、E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)的表达,RT-PCR检测PC-3细胞E-cadherin、N-cadherin及Ras、细胞外调节蛋白激酶(ERK)mRNA表达。结果与空白血清组比较,益肾通癃汤高、中、低剂量组均可显著抑制PC-3细胞增殖,降低其贴壁生长能力,显著促进PC-3细胞凋亡,显著降低PC-3细胞体外侵袭、迁移能力(P<0.05,P<0.01),均呈剂量依赖性;Western blot结果显示,与空白血清组比较,益肾通癃汤高、中、低剂量组PC-3细胞中Snail、Ras、p-ERK1/2、ERK1/2、N-cadherin、基质金属蛋白酶-9蛋白表达均有一定程度下调,E-cadherin蛋白表达明显上调(P<0.05,P<0.01);RT-PCR结果显示,益肾通癃汤高、中、低剂量组PC-3细胞Ras、ERK1、N-cadherin mRNA表达下调,E-cadherin mRNA表达上调。结论益肾通癃汤可有效抑制前列腺癌PC-3细胞的增殖,促进其凋亡,抑制其侵袭及迁移能力及上皮间质转化进程,其作用机制可能与调控Ras/ERK信号通路有关。 展开更多
关键词 前列腺癌 益肾通癃汤 ras/erk信号通路 上皮间质转化 大鼠
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