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肿瘤坏死因子(TNF)及内毒素在急性肝衰竭发病机理中起重要作用,两者均可诱导内源性磷脂酶 A_2(PLA_2)活性增高,而 PLA_2可使细胞膜磷脂降解,导致膜流动性下降,引起组织损伤。前列腺素 E_1(PGE_1)为肝细胞保护剂,它不仅能抑制枯否氏细胞及巨噬细胞合成 TNF,还可降低细胞膜的微粘度,改善膜的流动性,推测 PGE_1的保护肝细胞作用与降低 TNF 合成及PLA_2活性有关。为此,我们应用 D-氨基半乳糖及内毒素复制急性肝坏死动物模型,观察 PGE_1对其血清中 TNF 水平及肝组织匀浆中 PLA_2活性的影响,探讨 PGE_1保扩肝细胞的作用机制。结果显示,PGE_1治疗组动物血清中 TNF 含量为0.84±0.45(ng/ml),肝组织匀浆中 PLA_2活性为81.48±62.48(U),丙氨酸转氨酶(ALT)为806.67±621.39(U),天门冬氨酸转氨酶
Tumor necrosis factor (TNF) and endotoxin play an important role in the pathogenesis of acute liver failure, both of which can induce the increase of endogenous phospholipase A2 (PLA2) activity, while PLA2 can degrade the phospholipid of cell membrane, resulting in the decrease of membrane fluidity , Causing tissue damage. Prostaglandin E_1 (PGE_1) is a protective agent of hepatocytes, which not only inhibits the synthesis of TNF in Kupffer cells and macrophages, but also decreases the microviscosity of the cell membrane and improves the fluidity of the membrane, suggesting that PGE_1 may play a role in the protection of hepatocytes TNF synthesis and PLA 2 activity. To this end, we used D-galactosamine and endotoxin to replicate acute liver necrosis in animal models to observe the effect of PGE 1 on serum TNF levels and PLA 2 activity in liver homogenates, and to explore the mechanism of action of PGE 1 hepatocytes. The results showed that the content of TNF in the serum of PGE_1 treatment group was 0.84 ± 0.45 (ng / ml), the activity of PLA2 in liver homogenate was 81.48 ± 62.48 (U) and the alanine aminotransferase (ALT) was 806.67 ± 621.39 (U) , Aspartate aminotransferase