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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(P<0.01),受损细胞明显增多,ALT、IL-1β含量增多(P<0.01),TLR4和NF-κB p65表达水平显著提高(P<0.01),p65入核细胞比例提高(P<0.01)。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(P<0.01),受损细胞减少,ALT、IL-1β含量降低(P<0.01),TLR4和NF-κB p65表达水平明显降低(P<0.01),p65入核细胞比例下降(P<0.01)。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。
Objective To investigate the protective effect of resveratrol (RES) on hepatocyte injury induced by hypoxia / reoxygenation (H / R) in rats and its related molecular mechanisms. Methods The H / R model of BRL-3A cells (rat hepatocyte cell line) was established. Cells were pretreated with RES and TLR4 inhibitors (HTA125) before modeling. After modeling, cell viability and apoptosis were detected, cell morphological changes were observed, alanine transaminase (ALT) and inflammatory cytokines were detected in cell culture medium, mRNA and protein levels of TLR4 and NF-κB p65 Expression and NF-κB p65 into the nuclear situation. Results H / R conditions significantly decreased cell viability, increased apoptosis (P <0.01), increased damaged cells, increased levels of ALT and IL-1β (P <0.01), and expressions of TLR4 and NF-κB p65 (P <0.01), and the percentage of p65 in nucleated cells increased (P <0.01). After pretreatment with RES and HTA125, the cell viability was significantly increased, the proportion of apoptotic cells was significantly reduced (P <0.01), the number of damaged cells was decreased, the contents of ALT and IL-1β were decreased (P <0.01), TLR4 and NF- The expression of p65 was significantly decreased (P <0.01), and the percentage of p65 nuclear into cells decreased (P <0.01). Conclusion RES can reduce the injury of BRL-3A hepatocytes induced by H / R, which may be related to the inhibition of TLR4 / NF-κB signaling pathway.