肝细胞生长因子对四氯化碳损伤原代培养大鼠肝细胞的保护作用

采用大鼠离体肝细胞原代培养24 h，并利用CCl₄造成急性肝细胞损伤模型，检定肝细胞生长因子(HGF)对肝细胞损伤的影响. 结果表明：HGF可显著降低中毒肝细胞及细胞膜脂质过氧化物水平, 抑制肝细胞脂质过氧化, 并降低谷丙转氨酶和谷草转氨酶水平, 稳定质膜；显著促进中毒肝细胞RNA和DNA的合成；超微病理证实HGF能减轻CCl₄对肝细胞质膜，染色质, 线粒体, 内质网及核蛋白体的损害.

Protective effect of hepatocyte growth factor on CCl4-induced injury of primary cultured rat hepatocytes

In the present study, we examined the effect of hepatocyte growth factor (HGF) on CCl₄-intoxicated primary cultured rat hepatocytes. HGF (300 mg·L^-1) significantly lessened CCl₄(10 mmol·L^-1)-induced hepatocyte damage by decreasing GPT and GOT leakage and malondialdehyde (MDA) production. HGF significantly promoted [³H]uridine incorporation of RNA and [³H]thymidine incorporation of DNA in rat hepatocytes, and there was a good correlation between intracellular K⁺ leakage and [³H]uridine incorporation of RNA in HGF treated hepatocytes (y=-28.9+1262.9x, r=0.98, P<0.01). Cytopathological study showed that HGF was able to lessen injuries of heterochromatin, mitochondrion, endoplasmic reticulum and ribosome. In summary, HGF protects hepatocytes from CCl₄-induced hepatotoxicity. It is suggested that one of the mechanisms for this protection may be that HGF is able to stabilize plasmic membrane by inhibiting lipid peroxidation and to promote RNA and DNA synthesis of rat hepatocytes as well.