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作 者:朱文珍 冯慢慢 李浩然 迟晓琦 韩晓华[1] ZHU Wenzhen;FENG Manman;LI Haoran;CHI Xiaoqi;HAN Xiaohua(Department of Physiology, School of Basic Medicine, Qingdao University, Qingdao 266071, China)
机构地区:[1]青岛大学基础医学院生理学与病理生理学学系,山东青岛266071
出 处:《青岛大学学报(医学版)》2020年第2期190-193,共4页Journal of Qingdao University(Medical Sciences)
基 金:山东省自然科学基金项目(ZR2019MH110);青岛市民生科技计划项目(19-6-1-19-nsh)。
摘 要:目的探讨ANO1抑制剂T16A inh-A01(A01)对血管紧张素Ⅱ(AngⅡ)诱导的血管平滑肌细胞(VSMC)增殖及细胞外调节蛋白激酶(ERK)信号通路蛋白的影响。方法用AngⅡ、A01处理VSMC 24 h,采用四甲基偶氮唑蓝(MTT)法检测细胞存活率,采用Western blot法检测增殖细胞核抗原(PCNA)、磷酸化ERK(p-ERK)蛋白表达。结果与对照组相比,AngⅡ使细胞存活率升高至(121.2±2.4)%,10~20μmol/L A01能够明显抑制该作用(F=63.64,P<0.01)。AngⅡ处理细胞后,PCNA蛋白表达水平升高,该效应可被20μmol/L A01部分抑制(F=15.82,P<0.01)。此外,AngⅡ还增加了p-ERK蛋白的表达,该作用也可被A01显著抑制(F=36.01,P<0.01)。结论A01对AngⅡ诱导的VSMC增殖具有抑制作用,该作用可能与激活ERK信号通路相关。Objective To investigate the effect of ANO1 inhibitor T16A inh-A01(A01)on angiotensinⅡ(AngⅡ)-induced proliferation of vascular smooth muscle cells(VSMCs)and extracellular regulated protein kinase(ERK)signaling pathway proteins.Methods VSMCs were treated with AngⅡand A01,respectively,for 24 h.The survival rate of cells was determined by MTT assay,and the protein expression of proliferating cell nuclear antigen(PCNA)and phosphorylated ERK(p-ERK)was determined by Western blot.Results AngⅡincreased the survival rate of cells to 121.2%±2.4%(as compared with that of the control group),which could be significantly inhibited by 10-20μmol/L A01(F=63.64,P<0.01).After the cells were treated with AngⅡ,the protein expression level of PCNA was increased,which could be partially inhibited by 20μmol/L A01(F=15.82,P<0.01).In addition,AngⅡincreased the protein expression of p-ERK,which could also be significantly inhibited by A01(F=36.01,P<0.01).Conclusion A01 can inhibit AngⅡ-induced proliferation of VSMCs,which may be related to activation of the ERK signaling pathway.
关 键 词:ANO1抑制剂 血管紧张素Ⅱ 血管 肌细胞 平滑肌 细胞增殖
分 类 号:R544[医药卫生—心血管疾病] R329.25[医药卫生—内科学]
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