矢车菊素-3-O-葡糖苷干预核因子-κB通路抑制过氧化氢诱导的细胞凋亡  

Corncornin-3-O-glucoside mediates the NF-κB pathway to inhibit HO-induced apoptosis

作　　者：刘迪 于子翔 张寒雪 孙宏宇 郑美玉 时文艳 冯宪敏 Liu Di;Yu Zixiang;Zhang Hanxue;Sun Hongyu;Zheng Meiyu;Shi Wenyan;Feng Xianmin(Academy of Basic Medicine,Jilin Medical University,Jilin 132013,China;Academy of Medical Technology,Beihua University,Jilin 132013,China)

机构地区：[1]吉林医药学院基础医学院,吉林132013 [2]北华大学医学技术学院,吉林132013

出　　处：《卫生研究》2020年第5期775-779,801,共6页Journal of Hygiene Research

基　　金：吉林省自然科学基金(No.20200201146JC);吉林省科技发展计划(No.20190103148JH);吉林省卫生健康科技能力提升计划(No.2019Q031)。

摘　　要：目的研究矢车菊素-3-O-葡萄糖苷(cyanidin-3-O-glucoside,C3G)对H2O2诱导人胚肾细胞(human embryonic kidney 293 cells,HEK-293)损伤的抗凋亡作用。方法以0.4 mmol/L H2O2诱导HEK-293细胞凋亡,1.25、5、20μmol/L C3G预处理,检测凋亡细胞乳酸脱氢酶(lactate dehydrogenase,LDH)释放率和线粒体膜电位,免疫印迹法和反转录定量PCR(qRT-PCR)检测核因子(nuclear factor,NF)-κB凋亡信号通路中P65蛋白和mRNA表达量。结果 H2O2损伤细胞后,LDH释放率提高[(100±5.53)%比(57.28±4.83)%],线粒体膜电位下降[(55.97±1.89)%比100%],P65蛋白[(122.73±7.45)%比100%]和mRNA[1.66±0.06比1.00]表达均显著上调,差异均有统计学意义(P<0.05)。1.25、5、20μmol/L C3G预处理损伤细胞后,LDH释放率显著降低,分别为(81.59±2.49)%、(76.34±1.72)%和(69.69±3.46)%(P<0.05);线粒体膜电位呈浓度依赖性升高,分别为(66.05±2.47)%、(71.62±3.66)%和(77.42±2.71)%,各组间差异均有统计学意义(P<0.05);NF-κB通路中P65蛋白和mRNA表达均下调,分别为(71.16±8.71)%、(62.67±9.46)%和(43.74±6.23)%,以及(1.28±0.03)、(1.17±0.03)和(0.99±0.08)(P<0.05)。结论矢车菊素-3-O-葡萄糖苷对H2O2诱导的HEK-293细胞损伤具有抗凋亡作用,其作用机制可能是通过保护细胞生物膜,抑制NF-κB信号通路的激活实现抗凋亡作用。OBJECTIVE To study the anti-apoptotic effect of cyanidin-3-O-glucoside(C3 G) on H2O2-induced injury in human embryonic kidney(HEK)-293 cells. METHODS Hydrogen peroxide induced injury of HEK-293 cell was used as the research object. HEK-293 cells were pretreated with different concentrations of C3 G(1.25, 5, 20 μmol/L). The anti-apoptotic effects of C3 G on injured cells were examined by the release rates of LDH and mitochondrial membrane potential(MMP). Western blot and qRT-PCR were used to detect the protein expression and mRNA expression of NF-κB P65. RESULTS The result showed that the release rate of LDH was increased, MMP was decreased, the protein and mRNA of P65 was increased after H2O2 inducing. Whereas, the release rates of LDH were significantly lower than that of the injured group after 1.25, 5, 20 μmol/L C3 G pretreatment of injured cells(P<0.05). The MMP of C3 G group was significantly higher than injured group with concentration-dependent increases. The proteins and mRNA of P65 were also significantly lower than that of injured group(P<0.05). CONCLUSION Cyanidin-3-O-glucoside shows anti-apoptotic effect on H2O2-induced injury in HEK-293 cell. The mechanisms of anti-apoptotic effects may be to achieve by protecting cell biofilms, and inhibiting the activity of NF-κB signaling pathway.

关 键 词：矢车菊素-3-O-葡糖苷 抗细胞凋亡 人胚肾细胞 核因子-ΚB P65 

分 类 号：Q593[生物学—生物化学] Q946.836