白藜芦醇在缺氧/复氧诱导的肝细胞损伤中的保护作用及与TLR4/NF-κB通路的关系

何雕; 张国庆; 郑道峰; 魏续福; 刘锐; 吴忠均

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白藜芦醇在缺氧/复氧诱导的肝细胞损伤中的保护作用及与TLR4/NF-κB通路的关系

基础医学 | 更新时间：2026-01-09

- 白藜芦醇在缺氧/复氧诱导的肝细胞损伤中的保护作用及与TLR4/NF-κB通路的关系
- Resveratrol protects hepatocytes against hypoxia/reoxygenation injury and its relationship with TLR4/NF-κB pathway
- 陆军军医大学学报 2016年38卷第12期页码：1398-1403
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  中图分类号： R285.5;R322.47;R364.4
- 纸质出版：2016
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何雕,张国庆,郑道峰,魏续福,刘锐,吴忠均.白藜芦醇在缺氧/复氧诱导的肝细胞损伤中的保护作用及与TLR4/NF-κB通路的关系[J].陆军军医大学学报(原第三军医大学学报),2016,38(12):1398-1403.

　He Diao,Zhang Guoqing,Zheng Daofeng,Wei Xufu,Liu Rui,Wu Zhongjun.Resveratrol protects hepatocytes against hypoxia/reoxygenation injury and its relationship with TLR4/NF-κB pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(12):1398-1403.
何雕,张国庆,郑道峰,魏续福,刘锐,吴忠均.白藜芦醇在缺氧/复氧诱导的肝细胞损伤中的保护作用及与TLR4/NF-κB通路的关系[J].陆军军医大学学报(原第三军医大学学报),2016,38(12):1398-1403. DOI：

　He Diao,Zhang Guoqing,Zheng Daofeng,Wei Xufu,Liu Rui,Wu Zhongjun.Resveratrol protects hepatocytes against hypoxia/reoxygenation injury and its relationship with TLR4/NF-κB pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(12):1398-1403. DOI：

摘要

目的探讨白藜芦醇（resveratrol，RES）在缺氧/复氧（hypoxia reoxygenation，H/R）诱导的大鼠肝细胞损伤中的保护作用及其相关分子机制。方法建立BRL-3A细胞（大鼠肝细胞株）H/R模型。建模前分别用RES和TLR4抑制剂（HTA125）预处理细胞。建模完成后

检测细胞存活率及细胞凋亡，观察细胞形态变化，检测细胞培养液中谷丙转氨酶（alanine transaminase

ALT)及炎症因子含量，检测细胞TLR4、NF-κB p65基因mRNA及蛋白水平表达及NF-κB p65入核情况。结果 H/R条件使细胞存活率明显降低，细胞凋亡率增加（P0.01），受损细胞明显增多，ALT、IL-1β含量增多（P0.01），TLR4和NF-κB p65表达水平显著提高（P0.01），p65入核细胞比例提高（P0.01）。经RES及HTA125预处理后，细胞存活率显著提高，细胞凋亡比例显著缩小（P0.01），受损细胞减少，ALT、IL-1β含量降低（P0.01），TLR4和NF-κB p65表达水平明显降低（P0.01），p65入核细胞比例下降（P0.01）。结论 RES可以减轻H/R诱导的BRL-3A肝细胞损伤，该作用可能与抑制TLR4/NF-κB信号通路有关。

Abstract

Objective To determine the protective effect of resveratrol (RES) on hepatocytes induced by hypoxia/reoxygenation (H/R) and investigate the molecular mechanism. Methods Before H/R model was established

BRL-3A cells were treated with RES or HTA125 (TLR4 inhibitor). Survival rate and apoptosis were detected in the cells. Alanine transaminase (ALT) and interleukin-1β (IL-1β) in the culture were determined. The mRNA and protein expression levels of TLR4 and NF-κB p65 in the cells were determined by quantitative real-time PCR and Western blotting. Results H/R stimulation decreased cell survival rate and enhanced the apoptosis (P0.01). The expression levels of ALT and IL-1β were enhanced significantly (P0.01)

and the expression levels of TLR4 and NF-κB p65 were markedly increased (P0.01). After pretreatment with RES or HTA125

the cell survival rate was increased (P0.01) while the apoptosis decreased (P0.01). ALT and IL-1β were reduced significantly (P0.01)

and the expression levels of TLR4 and NF-κB p65 were decreased (P0.01). Moreover

RES inhibited the translocation of NF-κB p65 after H/R stimulation in BRL-3A cells (P0.01). Conclusion RES can alleviate the hepatocyte injury induced by H/R

which may be related with inhibition of TLR4/NF-κB signaling pathway.

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