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血管紧张素Ⅱ2型受体活化促进缺氧/复氧损伤PC12细胞的生长 被引量:1

Angiotensin Ⅱ type 2 receptor activation promotes the growth of PC12 cells induced by hypoxia/reoxygenation
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摘要 目的探讨血管紧张素Ⅱ2型受体(AT2R)活化对缺氧/复氧(H/R)损伤PC12细胞生长的影响。方法 PC12细胞是大鼠肾上腺嗜铬细胞瘤细胞株,具有神经内分泌细胞的一般特征。将PC12细胞用连二亚硫酸钠(Na_2S_2O_4)处理后复制H/R损伤的神经细胞模型;H/R损伤PC12细胞分别予以AT2R拮抗剂(PD123319)、AT2R激动剂(CGP42112)进行处理,采用MTT法观察细胞存活率的变化;以逆转录—聚合酶链式反应(RT-PCR)检测Bax、Bcl-2 mRNA表达的变化。结果 PC12细胞经40mmol/LNa_2S_2O_4处理1 h后,MTT法检测的细胞存活率约为55~60%,提示复制H/R损伤模型成功;H/R损伤PC12细胞经CGP42112处理后,细胞存活率显著增高,而Bax mRNA表达下调,Bcl-2 mRNA表达上调;而PD123319处理后,细胞存活率显著下降,Bax mRNA表达上调,Bcl-2 mRNA表达则下调。结论 AT2R活化可改善H/R损伤的PC12细胞的生长,其机理可能与其上调Bcl-2/Bax的比值有关。 Objective To investigate the effects of activated angiotensin II type 2 receptor( AT2R) on the growth of PC12 cells induced by hypoxia/reoxygenation( H/R). Methods PC12 cells were treated with Na_2S_2O_4 for 1 h to establish the H/R model.Then the cells were treated with AT2 R antagonist( PD123319) or AT2R agonist( CGP42112),respectively.The survival rate of cells was observed by MTT,the expression of Bax/Bcl-2 mRNA was detected through reverse transcription PCR. Results The survival ratio of cells is about 55 ~ 60% in the cells treated with 40 mmol/L Na_2S_2O_4 and shows that the H/R injury model is successfully established in the PC12 cells.Compared with the control groups,the survival rate of cells is increased,Bax mRNA expression is down-regulated and Bcl-2 mRNA expression is up-regulated in the H/R injury PC12 cells treated with CGP42112.While in the H/R injury PC12 cells treated with PD123319,the survival rate of cells is decreased,Bax mRNA expression is up-regulated and Bcl-2 mRNA expression is down-regulated. Conclusion AT2R activation can improve the growth of PC12 cells damaged by H/R,which the mechanism is related with the upregulation of Bcl-2/Bax ratio.
出处 《中南医学科学杂志》 CAS 2017年第1期35-41,共7页 Medical Science Journal of Central South China
基金 湖南省自然科学基金(2016JJ6133) 南华大学大学生研究性学习和创新性实验计划项目(2016NH053XJXZ)
关键词 血管紧张素Ⅱ2型受体 PC12细胞 缺氧/复氧损伤 凋亡 angiotensin Ⅱ type 2 receptor PC12 cells hypoxia/reoxygenation injury apoptosis
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