成纤维细胞生长因子21对内质网应激诱导心肌细胞凋亡的影响及其机制研究
发布时间：2018-12-12 16:29
【摘要】：目的:探讨成纤维细胞生长因子21(FGF21)在内质网应激(ERS)诱导心肌细胞凋亡中的保护作用及其作用机制。方法:以pc DNA4为基因载体,构建pc DNA4-FGF21质粒并转染H9c2大鼠心肌细胞48h,加入衣霉素(TM)10μM处理24h构建内质网应激模型,实验分为4个组:对照组、衣霉素处理组、pcDNA4-FGF21+衣霉素组、pcDNA4+衣霉素组。利用蛋白免疫印迹(Western blot)方法检测FGF21蛋白及蛋白激酶R样ER激酶(PERK)和c-Jun氨基末端激酶(JNK)介导的凋亡通路相关蛋白的表达。利用CCK8检测细胞存活率和TUNEL检测细胞凋亡率。结果:成功构建pcDNA4-FGF21质粒并在H9c2细胞中过表达。与对照组相比,衣霉素处理组和pcDNA4+衣霉素组明显上调H9c2细胞内源性FGF21的表达(P0.01),以及增加PERK和JNK介导的凋亡通路相关蛋白的表达(P0.05~0.01),减少细胞存活率和提高细胞凋亡水平(P0.05~0.01)。与衣霉素处理组和pcDNA4+衣霉素组相比,在pcDNA4-FGF21+衣霉素组明显降低PERK和JNK介导的凋亡通路相关蛋白的表达,增加细胞存活率,降低细胞凋亡水平(P0.05~0.01)。结论:FGF21过表达可以减轻内质网应激诱导心肌细胞的凋亡,其机制可能部分与抑制内质网应激中PERK和JNK介导促凋亡通路的信号传导有关。
[Abstract]:Aim: to investigate the protective effect of fibroblast growth factor 21 (FGF21) on cardiac myocyte apoptosis induced by endoplasmic reticulum stress (ERS) and its mechanism. Methods: pc DNA4 was used as gene vector, pc DNA4-FGF21 plasmid was constructed and transfected into H9c2 rat cardiomyocytes for 48 h. Endoplasmic reticulum stress model was established by adding 10 渭 M (TM) for 24 hours. The model was divided into four groups: control group and Itetracycline treated group. PcDNA4-FGF21 group and pcDNA4 group. Western blot (Western blot) was used to detect the expression of FGF21 protein, protein kinase R-like ER kinase (PERK) and c-Jun amino-terminal kinase (JNK) mediated apoptosis pathway. Cell survival rate was detected by CCK8 and apoptosis rate was detected by TUNEL. Results: pcDNA4-FGF21 plasmid was successfully constructed and overexpressed in H9c2 cells. Compared with the control group, the expression of endogenous FGF21 in H9c2 cells and the expression of PERK and JNK mediated apoptosis-related proteins in H9c2 cells were upregulated in the chlortetracycline and pcDNA4 groups (P0.05 / 0. 01). The cell survival rate was reduced and the apoptosis level was increased (P0.05N0.01). Compared with the pcDNA4-FGF21 group and the pcDNA4 group, the expression of apoptosis-related proteins mediated by PERK and JNK was significantly decreased, the cell survival rate was increased, and the apoptosis level was decreased in the pcDNA4-FGF21 group (P0.05 / 0. 01). Conclusion: overexpression of FGF21 can attenuate the apoptosis induced by endoplasmic reticulum stress, and its mechanism may be related to the inhibition of signal transduction mediated by PERK and JNK in endoplasmic reticulum stress.
【作者单位】： 青岛大学医学院附属烟台毓璜顶医院心内科;青岛大学医学院附属烟台毓璜顶医院生物芯片;青岛大学医学院附属烟台毓璜顶医院中心实验室;
【分类号】：R54
本文编号：2374909
[Abstract]:Aim: to investigate the protective effect of fibroblast growth factor 21 (FGF21) on cardiac myocyte apoptosis induced by endoplasmic reticulum stress (ERS) and its mechanism. Methods: pc DNA4 was used as gene vector, pc DNA4-FGF21 plasmid was constructed and transfected into H9c2 rat cardiomyocytes for 48 h. Endoplasmic reticulum stress model was established by adding 10 渭 M (TM) for 24 hours. The model was divided into four groups: control group and Itetracycline treated group. PcDNA4-FGF21 group and pcDNA4 group. Western blot (Western blot) was used to detect the expression of FGF21 protein, protein kinase R-like ER kinase (PERK) and c-Jun amino-terminal kinase (JNK) mediated apoptosis pathway. Cell survival rate was detected by CCK8 and apoptosis rate was detected by TUNEL. Results: pcDNA4-FGF21 plasmid was successfully constructed and overexpressed in H9c2 cells. Compared with the control group, the expression of endogenous FGF21 in H9c2 cells and the expression of PERK and JNK mediated apoptosis-related proteins in H9c2 cells were upregulated in the chlortetracycline and pcDNA4 groups (P0.05 / 0. 01). The cell survival rate was reduced and the apoptosis level was increased (P0.05N0.01). Compared with the pcDNA4-FGF21 group and the pcDNA4 group, the expression of apoptosis-related proteins mediated by PERK and JNK was significantly decreased, the cell survival rate was increased, and the apoptosis level was decreased in the pcDNA4-FGF21 group (P0.05 / 0. 01). Conclusion: overexpression of FGF21 can attenuate the apoptosis induced by endoplasmic reticulum stress, and its mechanism may be related to the inhibition of signal transduction mediated by PERK and JNK in endoplasmic reticulum stress.
【作者单位】： 青岛大学医学院附属烟台毓璜顶医院心内科;青岛大学医学院附属烟台毓璜顶医院生物芯片;青岛大学医学院附属烟台毓璜顶医院中心实验室;
【分类号】：R54
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