血管紧张素Ⅱ对肝癌细胞增殖的影响及其机制研究  

Effect of angiotensinⅡon the proliferation of hepatoma cells and its mechanism

作　　者：全裔[1] 杨峻[1] 农林琳[2] 王秀娟 王丽兰 胡玉芳[4] QUAN Yi;YANG Jun;NONG Lin-lin;WANG Xiu-juan;WANG Li-lian;HU Yu-fang(Department of Laboratory,Affiliated Hospital of Guilin Medical College,Guilin Guangxi 541001;Academic Institute,Guilin Medical College,Guilin Guangxi 541001,China;Medical Laboratory Institute,Guilin Medical College,Guilin Guangxi 541001,China;Department of Radiology,Affiliated Hospital of Guilin Medical College,Guilin Guangxi 541001)

机构地区：[1]桂林医学院附属医院检验科,广西桂林541001 [2]桂林医学院基础医学院,广西桂林541001 [3]桂林医学院医学检验学院,广西桂林541001 [4]桂林医学院附属医院放射科,广西桂林541001

出　　处：《蚌埠医学院学报》2022年第1期18-21,共4页Journal of Bengbu Medical College

基　　金：广西高校中青年教师科研基础能力提升项目(2019KY0536)。

摘　　要：目的:研究血管紧张素Ⅱ对肝癌HepG2细胞增殖的影响及其机制。方法:采用CCK-8法测定不同浓度血管紧张素Ⅱ作用24、48 h对HepG2细胞增殖的影响。通过蛋白质免疫印迹法测定血管紧张素Ⅱ处理后HepG2细胞内细胞外信号调节激酶(ERK)1/2和血管紧张素Ⅱ-1型受体(AT1R)蛋白表达水平。结果:作用24 h,10^(-6)、10^(-5) mol/L血管紧张素Ⅱ处理的HepG2细胞吸光度值均高于对照组(P<0.05);10^(-5) mol/L血管紧张素Ⅱ处理的HepG2细胞吸光度值高于10^(-8) mol/L血管紧张素Ⅱ组(P<0.05)。作用48 h,10^(-8)、10^(-7)、10^(-6)、10^(-5)、10^(-4) mol/L血管紧张素Ⅱ处理的HepG2细胞吸光度值均高于对照组(P<0.05)。10^(-7)、10^(-6)、10^(-5)、10^(-4) mol/L血管紧张素Ⅱ处理的HepG2细胞中AT1R蛋白表达水平均高于对照组(P<0.05)。10^(-8)、10^(-6)、10^(-5)、10^(-4) mol/L血管紧张素Ⅱ各亚组比较,HepG2细胞AT1R蛋白表达随着药物浓度的升高而升高(P<0.01)。10^(-6) mol/L血管紧张素Ⅱ处理HepG2细胞5、10、20、30 min后ERK1/2蛋白表达量并无明显改变(P>0.05),而在处理5、10 min后磷酸化ERK1/2蛋白表达量高于0、20、30 min(P<0.05)。结论:血管紧张素Ⅱ可能通过上调AT1R的蛋白表达,促进ERK1/2磷酸化,以促进肝癌HepG2细胞异常增殖。Objective:To study the effect of angiotensinⅡon the proliferation of hepatoma HepG2 cells and its mechanism.Methods:CCK-8 method was used to determine the effects of different concentrations of angiotensinⅡon the proliferation of HepG2 cells treated for 24 and 48 hours.The expression levels of extracellular signal regulated kinase(ERK)1/2 and angiotensinⅡtype 1 receptor(AT1R)in HepG2 cells treated with angiotensinⅡwere measured by Western blotting.Results:The absorbance values of HepG2 cells treated with 10^(-6) and 10^(-5) mol/L angiotensinⅡfor 24 hours were higher than those in control group(P<0.05),which in 10^(-5) mol/L angiotensinⅡgroup was higher than that in 10^(-8) mol/L angiotensinⅡgroup(P<0.05).The absorbance values of HepG2 cells treated with 10^(-8),10^(-7),10^(-6),10^(-5) and 10^(-4) mol/L angiotensinⅡfor 48 hours were higher than those in control group(P<0.05).The expression levels of AT1R protein in HepG2 cells treated with 10^(-7),10^(-6),10^(-5) and 10^(-4) mol/L angiotensinⅡwere higher than those in the control group(P<0.05).Among the 10^(-8),10^(-6),10^(-5) and 10^(-4) mol/L angiotensinⅡgroups,the expression of AT1R protein in HepG2 cells increased with the increase of drug concentration(P<0.01).The expression of ERK1/2 protein in HepG2 cells treated with 10^(-6) mol/L angiotensinⅡfor 5,10,20 and 30 minutes did not change significantly(P>0.05),but the expression of phosphorylated ERK1/2 protein treated for 5 and 10 minutes was higher than that for 0,20 and 30 minutes(P<0.05).Conclusions:AngiotensinⅡmay be through upregulating AT1R protein expression and promoting ERK1/2 phosphorylation to promote the abnormal proliferation of hepatoma HepG2 cells.

关 键 词：肝肿瘤 血管紧张素Ⅱ 细胞增殖 细胞外信号调节激酶 血管紧张素1型受体 

分 类 号：R734.2[医药卫生—肿瘤]