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作 者:万强[1,2] 潘芸芸[2] 贾钰华[2] 刘中勇[1]
机构地区:[1]江西中医药大学附属医院,江西南昌330006 [2]南方医科大学中医药学院,广东广州510515
出 处:《时珍国医国药》2015年第9期2061-2064,共4页Lishizhen Medicine and Materia Medica Research
基 金:国家自然科学基金项目(No.81373574;No.81460680);江西省科技计划项目(No.20135BBG7002);广东省广州市海珠区科技计划项目(No.2013-cg-35)
摘 要:目的观察三七皂苷R1(R1)对过氧化氢(H2O2)诱导心肌细胞损伤的保护作用及与JNK通路的关系。方法分离原代培养的乳鼠心肌细胞,加入H2O2构建心肌损伤模型,以不同质量浓度R1(25,50,100μmol·L-1)及JNK通路抑制剂SP600125作用心肌细胞,MTT法测细胞活力;流式细胞仪检测细胞凋亡;试剂盒测丙二醛(MDA)含量及过氧化物歧化酶(SOD)活性;Western blot测心肌细胞中p-JNK、Bax、Bcl-2蛋白相对表达。结果与对照组相比,H2O2能显著降低心肌细胞活力,增加心肌细胞凋亡率,增加心肌细胞内MDA含量,降低SOD活性,上调心肌细胞内p-JNK、Bax蛋白表达并减少Bcl-2蛋白表达(P<0.05);与模型组比,R1及SP600125均能显著提高心肌细胞活力,降低心肌细胞凋亡率,减少心肌细胞内MDA含量,提高SOD活性,降低心肌细胞内p-JNK、Bax蛋白表达并增加Bcl-2蛋白表达(P<0.05)。结论R1可显著减轻H2O2诱导的心肌细胞损伤,其机制与抑制JNK通路的激活有关。Objective To study the protective effects of Notoginsenoside R1 in reducing cardiomyocytes injury induced by hydrogen peroxide through e -Jun N -terminal kinase (JNK) pathway. Methods Models of hydrogen peroxide -induced injury in car- diomyocytes from neonatal rats were established. Different concentrations of hydrogen peroxide (25, 50, 100 μmol · L^-1 ) and SP600125 were added in cardiomyocytes. MTr assay and flow cytometry were used to detect the viability and the apoptotic rate of cardiomyocytes, SOD activity and MDA content of cardiomyocytes by kits, the expressions of p - JNK, Bax and Bcl - 2 in eardiomyocytes were determined by Western blot. Results Compared with the control group, hydrogen peroxide can significantly decrease the activity and increase the apoptotic rate of cardiomyocytes, increased the MDA content and decreased the SOD activity in cardiomyocytes. Meanwhile, it can increase p - JNK and Bax expressions but decrease Bcl - 2 expression. Compared with the model group, Notoginsenoside R1 and SP600125 could increase the viability and decrease the apoptotic rate of cardiomyocytes, decrease the MDA content and increase the SOD activity in cardiomyoeytes, it could restrain p - JNK and Bax expressions but in- crease Bc] -2 expression in cardiomyoeytes. Conclusion Notoginsenoside R1 can reduce cardiomyocytes injury induced by hydrogen peroxide, the mechanism is related to the inhibition of JNK signal pathway activation.
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