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| 姜黄素-绿原酸对肝细胞氧化损伤的协同保护作用及机制研究 |
| Protective Effect of Curcumin Combined with Chlorogenic Acid on H2O2-induced Liver Injury and Its Mechanism |
| 投稿时间：2026-05-11 修订日期：2026-05-22 |
| DOI： |
| 中文关键词: 姜黄素-绿原酸复合物 L02肝细胞 氧化损伤 自噬 LC3B |
| 英文关键词:CUR-CGA complex, L02 liver cells, Oxidative damage autophagy, LC3B |
| 基金项目:江西省重点研发计划（20232BBG70017）和北京市自然科学基金（22JCZXJC00100） |
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| 中文摘要: |
| 探讨姜黄素-绿原酸复合物对L02肝细胞氧化应激损伤的协同保护作用及其潜在机制。利用体外培养的L02细胞,采用280μmol.L-1H2O2诱导L02细胞造模,诱导细胞氧化应激损伤；并同时将细胞分为对照组、H2O2诱导组、姜黄素实验组：H2O2+姜黄素(10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1)、绿原酸实验组：H2O2+绿原酸(10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1)、姜黄素-绿原酸协同组：H2O2+姜黄素-绿原酸(10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1)；各组分别给予相应浓度药物处理24 h后,采用CCK-8法检测细胞存活率,荧光显微镜观察线粒体膜电位(MMP)变化,实时荧光定量聚合酶链式反应(RT-qPCR)检测微管相关蛋白1轻链3(LC3B)mRNA表达水平,Western blot法检测LC3B蛋白表达水平。分析结果显示,与模型组相比,姜黄素-绿原酸复合组可显著提高受损L02细胞的存活率(P＜0.01或P＜0.05),提高线粒体膜电位水平(P＜0.01或P＜0.05),同时显著上调LC3B mRNA及蛋白表达水平(P＜0.01或P＜0.05)。根据结果我们认为,姜黄素-绿原酸复合物可有效改善氧化应激损伤细胞的线粒体功能,同时上调自噬相关基因LC3B的表达,激活自噬相关蛋白LC3B的活性水平,进而对H?O?诱导L02肝细胞的氧化应激损伤起到协同保护作用。 |
| 英文摘要: |
| To investigate the protective mechanism of curcumin(CUR) and chlorogenic acid(CGA) complex on the antioxidative damage in L02 liver cells. L02 cells were cultured in vitro, followed by 24-hour treatment with 280μmol.L-1 H2O2 to induce the oxidative damage model of the cells. And the cells were simultaneously divided into five group；control group, H2O2 model group,CUR group: H2O2+ CUR (10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1); CGA group: H2O2+CGA (10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1); CUR- CGA complex group: H2O2+ CUR-CGA complex (10μmol.L-1,25μmol.L-1,30μmol.L-1,40μmol.L-1);Every group were treated with H2O2 and different concentrations of CUR, CGA, and CUR-CGA complex for 24 hours. LO2 cells activity of every groups was detected with CCK-8 method, Mitochondrial membrane potential (MMP) was detected via Rhodamine 123 fluorescence staining method; the proteins and mRNA expression of LC3B was detected by western blot and RT-qPCR . The CUR-CGA complex can significantly improve the survival rate of injured cells (P<0.01 or P<0.05), increase the level of MMP (P<0.01 or P<0.05), The RT-qPCR and western blot result show that compared with the model group , significantly promote the expression level of LC3B mRNA in the CUR-CGA complex group cells (P<0.01 or P<0.05);and the expression level of LC3B protein was significantly upregulated (P<0.01),thus protecting hepatocytes. The mechanism of CUR-CGA complex protection against H2O2 induced oxidative damage in L02 liver cells may be related to improving mitochondrial function by promote the MMP and stimulating autophagy by increasing the expression of level of LC3B mRNA and protein. |
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