摘要
目的研究植物提取的京尼平(Genipin,GEN)对高浓度糖氧化损伤的大鼠心肌细胞系H9c2的影响作用。方法体外培养H9c2细胞4组,各组H9c2细胞存活率利用CCK-8法检测;AnnexinⅤ/PI双标记流式分析法检测细胞凋亡率;酶标法测定细胞上清液肌酸激酶(CK-MB)的水平,比色法和WST-1法分别测定细胞内丙二醛(MDA)含量和超氧化物歧化酶(SOD)活力。结果CCK-8法分析结果显示,33.3mmol/L高浓度糖条件下细胞存活率显著低于正常糖对照组,10μmol/L京尼平保护组细胞存活率高于高糖组(P<0.05)。AnnexinⅤ/PI双标记法检测高糖组细胞早期凋亡率显著高于正常糖组(P<0.05),而高糖加京尼平组比高糖组早期凋亡率显著降低(P<0.05)。京尼平保护组与高糖损伤组比较,上清液中CK-MB活性下降,细胞内MDA含量下降,SOD活力升高(P<0.05)。结论一定浓度的京尼平具有抗氧化保护高浓度糖损伤的H9c2心肌细胞的作用。
Objective To explore attenuate effects of genipin on high glucose-induced oxidative injury in H9c2 cells.Methods H9c2 cells were cultured in vitro and divided into four groups.We measured viability of H9c2 exposed to different concentrations of glucose by CCK-8 assay.The oxidative stress-induced early apoptosis of cells were analyzed by AnnexinⅤ/PI flow cytometry.The levels of CK-MB in the supernatant of culture media and the levels of MDA and SOD in the H9c2 cells were determined by colorimetry.Results CCK-8 assay results showed that the viability decreased with the 33.3 mmol/L glucose concentration,while the group pretreated with 10μmol/L genipin could increase the viability significantly(P<0.05).Compared with the control group,high glucose could induce cell oxidative stress-induced early apoptosis by AnnexinⅤ/PI flow cytometry,while genipin could inhibit the early apoptosis induced by high glucose significantly(P<0.05).The results showed significant increase of CK-MB and MDA levels and decrease of SOD activity in the high glucose group compared with the control group.However,the high glucose group pretreated with genipin,CK-MB and MDA levels decreased and SOD activity increased significantly compared with the high glucose group(P<0.05).Conclusion Genipin can attenuates significantly high glucose-induced oxidative injury in H9c2.
作者
师岩
陈庆友
刘玉宝
宁小美
张春晶
王小龙
李林
徐晶
张雪丽
Shi Yan;Chen Qingyou;Liu Yubao(Department of Biochemistry,Qiqihar Medical College,Heilongjiang 161006,China)
出处
《医学研究杂志》
2020年第9期164-168,共5页
Journal of Medical Research
基金
齐齐哈尔医学院院内科研基金资助项目(面上项目)(QMSI2017M-06)
黑龙江省大学生创新训练项目(201911230065)。
作者简介
通讯作者:师岩,电子信箱:94045545@qq.com。
