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本研究通过体外实验,探讨了内毒素对肝细胞脂质过氧化损伤的作用以及SOD的保护效应。用分离的大鼠肝细胞与内毒素(500ng/ml)共同孵育,6h肝细胞MDA、LDH和SOD水平均显著上升(P<0.05～0.01),而且LDH和SOD升高早于MDA;预先将PMN经内毒素处理后,再与肝细胞共孵,激活的PMN能显著损伤肝细胞,引起肝细胞MDA升高和LDH释放增加(P<0.01),SOD活性下降(P<0.05)。给予SOD治疗能部分抑制PMN对肝细胞的损伤作用。上述结果提示,内毒素对PMN引起肝细胞的损伤具有增强作用,内毒素亦可直接诱导肝细胞脂质过氧化损伤,但其机制尚待进一步阐明。
In this study, in vitro experiments to explore the role of endotoxin on lipid peroxidation in liver cells and the protective effect of SOD. Incubation of isolated rat hepatocytes with endotoxin (500ng / ml) significantly increased the levels of MDA, LDH and SOD at 6h (P <0.05-0.01), and LDH and SOD increased earlier than MDA PMN was endotoxin-treated, and then incubated with hepatocytes. The activated PMN could significantly damage the hepatocytes, cause increased MDA and increase the release of LDH (P <0.01) and decrease the activity of SOD in hepatocytes (P <0.05). The treatment with SOD could partially inhibit the damage of PMN to hepatocytes. The above results suggest that endotoxin can enhance the damage of liver cells induced by PMN, and endotoxin can directly induce lipid peroxidation injury in liver cells, but its mechanism needs to be further elucidated.