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低聚葡萄籽原花青素对顺铂所致人胚肾细胞线粒体损伤的保护作用  ( EI收录)  

Protective Effect of Oligomeric Grape Seed Proanthocyanidins on Cisplatin-Induced Mitochondrial Damage in HEK293 Cells

文献类型:期刊文献

中文题名:低聚葡萄籽原花青素对顺铂所致人胚肾细胞线粒体损伤的保护作用

英文题名:Protective Effect of Oligomeric Grape Seed Proanthocyanidins on Cisplatin-Induced Mitochondrial Damage in HEK293 Cells

作者:韩何丹[1];杜月梅[1];王海[1];赵艳萌[1];高丽萍[1]

第一作者:韩何丹

通讯作者:Gao, Liping

机构:[1]北京联合大学生物化学工程学院生物活性物质与功能食品北京市重点实验室

第一机构:北京联合大学生物化学工程学院|北京联合大学应用文理学院

年份:2020

卷号:41

期号:1

起止页码:168-174

中文期刊名:食品科学

外文期刊名:Food Science

收录:CSTPCD;;EI(收录号:20201008264674);Scopus;北大核心:【北大核心2017】;CSCD:【CSCD_E2019_2020】;

基金:北京市自然科学基金项目(7163211)

语种:中文

中文关键词:低聚葡萄籽原花青素;顺铂;人胚肾细胞HEK293;线粒体;凋亡

外文关键词:oligomeric grape seed proanthocyanidins;cisplatin;HEK293 cells;mitochondria;apoptosis

摘要:目的:探究低聚葡萄籽原花青素(oligomeric grape seed proanthocyanidins,O-GSP)对顺铂(cis-diamminedichloroplatinum,CDDP)导致的人胚肾细胞HEK293中线粒体损伤的保护作用及其作用机制。方法:通过试剂盒检测O-GSP、CDDP及O-GSP+CDDP处理后细胞中丙二醛(malondialdehyde,MDA)、还原型谷胱甘肽(glutathione,GSH)、活性氧(reaction oxygen species,ROS)含量、细胞质内糖代谢酶(己糖激酶和乳酸脱氢酶)活力和线粒体糖代谢酶(苹果酸脱氢酶)活力变化情况,并采用流式细胞术对各组细胞ATP含量、线粒体膜电位变化以及细胞凋亡率进行检测。结果:O-GSP预处理极显著改善了CDDP引起的细胞内MDA含量升高,还原型GSH、ROS、ATP含量及线粒体膜电位降低和糖代谢异常(P<0.01),从而减轻了CDDP诱发的线粒体损伤,对HEK293细胞凋亡有极显著的缓解作用(P<0.01)。结论:O-GSP对CDDP所致HEK293细胞线粒体损伤具有拮抗作用,并且该作用与O-GSP的抗氧化活性有关。
Objective: To investigate the protective effect and underlying mechanism of oligomeric grape seed proanthocyanidins(O-GSP) on cisplatin(CDDP)-induced mitochondrial damage in HEK293 cells. Methods: The contents of malondialdehyde(MDA), reduced glutathione(GSH) and reactive oxygen species(ROS) and the activities of hexokinase(HK), lactate dehydrogenase(LDH) and malic dehydrogenase(MDH) were measured with relative reagent kit, and the ATP level, mitochondrial membrane potential and apoptosis rate in HEK293 cells treated by O-GSP and/or CDDP were determined by flow cytometry. Results showed that O-GSP pretreatment significantly attenuated the changes in MDA, reduced GSH and ROS contents caused by CDDP. Moreover, O-GSP significantly inhibited the decrease in ATP level and mitochondrial membrane potential and abnormal glucose metabolism induced by CDDP(P < 0.01), thus alleviating mitochondrial damage and reducing apoptosis in HEK293 cells(P < 0.01). Conclusion: O-GSP has an antagonistic effect on CDDP-induced mitochondrial damage in HEK293 cells, which is likely to be associated with the antioxidant activity of O-GSP.

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