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    全裔, 杨峻, 农林琳, 王秀娟, 王丽兰, 胡玉芳. 血管紧张素Ⅱ对肝癌细胞增殖的影响及其机制研究[J]. 蚌埠医科大学学报, 2022, 47(1): 18-21. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.004
    引用本文: 全裔, 杨峻, 农林琳, 王秀娟, 王丽兰, 胡玉芳. 血管紧张素Ⅱ对肝癌细胞增殖的影响及其机制研究[J]. 蚌埠医科大学学报, 2022, 47(1): 18-21. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.004
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    QUAN Yi, YANG Jun, NONG Lin-lin, WANG Xiu-juan, WANG Li-lian, HU Yu-fang. Effect of angiotensin Ⅱ on the proliferation of hepatoma cells and its mechanism[J]. Journal of Bengbu Medical University, 2022, 47(1): 18-21. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.004
    Citation: QUAN Yi, YANG Jun, NONG Lin-lin, WANG Xiu-juan, WANG Li-lian, HU Yu-fang. Effect of angiotensin Ⅱ on the proliferation of hepatoma cells and its mechanism[J]. Journal of Bengbu Medical University, 2022, 47(1): 18-21. DOI: 10.13898/j.cnki.issn.1000-2200.2022.01.004
    shu

    血管紧张素Ⅱ对肝癌细胞增殖的影响及其机制研究

    Effect of angiotensin Ⅱ on the proliferation of hepatoma cells and its mechanism

      摘要
    • 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。

       

      Abstract:
      ObjectiveTo study the effect of angiotensin Ⅱ on the proliferation of hepatoma HepG2 cells and its mechanism.
      MethodsCCK-8 method was used to determine the effects of different concentrations of angiotensin Ⅱ on the proliferation of HepG2 cells treated for 24 and 48 hours.The expression levels of extracellular signal regulated kinase(ERK) 1/2 and angiotensin Ⅱ type 1 receptor(AT1R) in HepG2 cells treated with angiotensin Ⅱ were measured by Western blotting.
      ResultsThe absorbance values of HepG2 cells treated with 10-6 and 10-5 mol/L angiotensin Ⅱ for 24 hours were higher than those in control group(P < 0.05), which in 10-5 mol/L angiotensin Ⅱ group was higher than that in 10-8 mol/L angiotensin Ⅱ group(P < 0.05).The absorbance values of HepG2 cells treated with 10-8, 10-7, 10-6, 10-5 and 10-4 mol/L angiotensin Ⅱ for 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 angiotensin Ⅱ were higher than those in the control group(P < 0.05).Among the 10-8, 10-6, 10-5 and 10-4 mol/L angiotensin Ⅱ groups, 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 angiotensin Ⅱ for 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).
      ConclusionsAngiotensin Ⅱ may be through upregulating AT1R protein expression and promoting ERK1/2 phosphorylation to promote the abnormal proliferation of hepatoma HepG2 cells.

       

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