雷公藤甲素减轻心肌细胞缺血再灌注损伤的研究OA
Triptolide attenuates myocardial ischemia-reperfusion injury
目的 探讨雷公藤甲素(Tri)减轻心肌细胞缺血再灌注(I/R)损伤的作用及机制.方法 将大鼠心肌H9c2细胞分为I/R组、I/R+Tri组和对照组,利用酶联免疫吸附试验测定反映H9c2细胞损伤的心肌酶学指标[肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)],反映H9c2细胞氧化应激水平的指标[活性氧,丙二醛和超氧化物歧化酶(SOD)].使用荧光定量PCR技术定量测定细胞凋亡相关基因[B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、肿瘤蛋白53(p53)、半胱氨酸天冬氨酸特异性蛋白酶-3(Caspase-3)]表达,使用蛋白质免疫印迹法测定细胞凋亡相关蛋白[Bax、Bcl-2、Caspase-3、剪切型Caspase-3(c-Caspase-3 表达].结果 I/R组、I/R+Tri组CK、LDH高于对照组,I/R组活性氧高于I/R+Tri组、对照组,差异均有统计学意义(均P<0.01).I/R组Bax、Caspase-3、c-Caspase-3相对表达水平及Bax/Bcl-2比值高于I/R+Tri组和对照组,I/R组Bcl-2相对表达水平低于I/R+Tri组和对照组,I/R+Tri组Bax、Caspase-3、c-Caspase-3相对表达水平及Bax/Bcl-2比值低于对照组,I/R+Tri组Bcl-2相对表达水平高于对照组,差异均有统计学意义(均P<0.01).结论 Tri可通过降低氧化应激程度、抑制线粒体相关的凋亡因子,减轻心肌细胞I/R.
Objective To investigate the effect and mechanism of triptolide(Tri)in alleviating ischemia/reperfusion(I/R)injury in cardiomyocytes.Methods H9c2 rat cardiomyocytes were divided into the I/R group,the I/R+Tri group,and the control group.The myocardial enzyme markers reflecting H9c2cell injury,including creatine kinase(CK),creatine kinase isoenzyme(CK-MB),and lactate dehydrogenase(LDH),as well as the indicators reflecting oxidative stress levels in H9c2 cells,including reactive oxygen species(ROS),malondialdehyde(MDA),and superoxide dismutase(SOD),were detected by ELISA.The expression levels of apoptosis-related genes(Bax,p53,Bcl-2,and Caspase-3)were determined by quantitative real-time polymerase chain reaction(qPCR),and the expression levels of apoptosis-related proteins[Bax,Bcl-2,Caspase-3,and cleaved Caspase-3(c-Caspase-3)]were measured by Western blot analysis.Results The levels of CK and LDH in the I/R group and the I/R+Tri group were higher than those in the control group,and the level of ROS in the I/R group was higher than those in the I/R+Tri group and the control group,with statistically significant differences(all P<0.01).The relative expression levels of Bax,Caspase-3,c-Caspase-3 and the Bax/Bcl-2 ratio in the I/R group were higher than those in the I/R+Tri group and the control group,while the relative expression level of Bcl-2 in the I/R group was lower than those in the I/R+Tri group and the control group.The relative expression levels of Bax,Caspase-3,c-Caspase-3 and the Bax/Bcl-2 ratio in the I/R+Tri group were lower than those in the control group,and the relative expression level of Bcl-2 in the I/R+Tri group was higher than that in the control group,with statistically significant differences(all P<0.01).Conclusion Tri can alleviate cardiomyocyte I/R injury by reducing oxidative stress and inhibiting mitochondria-related apoptotic factors.
赵圣刚;石晓雯;刘磊;李扬;张冉;韩集波;蒋芬芬;李澈;许建江
314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科314000 嘉兴大学附属第二医院心血管内科
雷公藤甲素缺血再灌注损伤氧化应激线粒体凋亡
TriptolideIschemia-reperfusion injuryOxidative stressMitochondriaApoptosis
《浙江医学》 2026 (10)
1025-1030,后插1,7
嘉兴市科技计划项目(2023AY40033)嘉兴市卫生科技计划项目(WKD25003)浙江省医药卫生科技计划项目(2019ZD055)
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