贵州医科大学学报

2019, v.44;No.221(02) 190-194

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雷公藤内酯醇保护心肌H/R损伤的相关分子机制
Study on the Molecular Mechanism of Triptolide Protective Effect on Myocardial H/R Injury

于海杰;关启刚;郭亮;张心刚;孙国哲;
YU Haijie;GUAN Qigang;GUO Liang;ZHANG Xingang;SUN Guozhe;The First Affiliated Hospital of China Medical University;

摘要(Abstract):

目的:探讨雷公藤内酯醇(TPL)对H9c2细胞缺氧/复氧(H/R)损伤的保护作用机制。方法:将体外培养的H9c2大鼠心肌细胞分为对照组、H/R组及TPL+H/R组,TPL+H/R组用TPL预处理48 h后,再进行H/R处理;各组细胞处理结束后,CCK-8法检测H9c2细胞增殖情况,ELISA法检测H9c2细胞培养上清液中MDA、SOD及促炎因子TNF-α、IL-6、IL-1β的含量,Western blot检测H9c2细胞中Nrf2、HO-1、TLR4、MyD88及胞核中NF-κB p65的表达水平。结果:与对照组相比,H/R组H9c2细胞增殖受到明显抑制,细胞上清液中MDA和促炎因子含量增加,SOD活力下降,Nrf2、HO-1、TLR4、MyD88及胞核中NF-κB p65蛋白表达水平均显著上调;与H/R相比,TPL+H/R组细胞增殖抑制情况得到缓解,细胞上清液中MDA与促炎因子含量下降,SOD活力上升,Nrf2、HO-1蛋白水平进一步上调,而TLR4、MyD88及胞核中NF-κB p65表达水平显著下降。结论:TPL可能通过激活Nrf2/HO-1信号通路提高心肌细胞抗氧化应激的能力,同时可能通过抑制TLR4/MyD88/NF-κB p65信号通路缓解炎症反应,从而发挥心肌保护作用。
Objective: To investigate the protective mechanism of triptolide( TPL) on hypoxia/reoxygenation( H/R) injury in H9 c2 cells. Methods: The H9 c2 rat cardiomyocytes cultured in vitro were divided into control group,H/R group and TPL + H/R group( H/R treatment after the treatment with TPL for 48 h). CCK8 assay was used to determine cell proliferation. MDA,SOD and pro-inflammatory cytokines TNF-α,IL-6,IL-1β content in cell supernatants were detected using the corresponding ELISA kit. Western blot analysis was used to detect the protein expression levels of Nrf2,HO-1,TLR4,MyD88 in cells and NF-κB p65 in nuclei. Results: When compared to control group,H/R treatment caused shrinkage of H9 c2 cells,increased the number of round suspended cells,and significantly inhibited cell proliferation. The levels of MDA and pro-inflammatory cytokines in cellular supernatants were increased by H/R treatment. The activity of SOD was decreased. The expression levels of Nrf2,HO-1,TLR4,MyD88 in whole cell lysates and NF-κB p65 in nuclei were significantly upregulated. When Compared with H/R, TPL treatment significantly reversed H/R-mediated effects.Conclusion: TPL may increase the ability of anti-oxidative stress in cardiomyocytes by further activating the Nrf2/HO-1 signaling pathway,and at the same time,inhibit the inflammatory response by inhibiting the TLR4/MyD88/NF-κB p65 signaling pathway,thereby protecting the myocardium.

关键词(KeyWords): 雷公藤内酯醇;心肌细胞;缺氧;复氧;氧化应激;炎症反应;信号传导
triptolide;cardiomyocytes;hypoxia;reoxygenation;oxidative stress;inflammatory response;signal transduction

Abstract:

Keywords:

基金项目(Foundation): 辽宁省自然科学基金资助项目(201602871)

作者(Author): 于海杰;关启刚;郭亮;张心刚;孙国哲;
YU Haijie;GUAN Qigang;GUO Liang;ZHANG Xingang;SUN Guozhe;The First Affiliated Hospital of China Medical University;

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DOI: 10.19367/j.cnki.1000-2707.2019.02.013

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