Wu B, Wang C, Xu J, Zhu J, Xu Y
Department of Gastroenterology, First Affiliated Hospital, Jiangxi Medical College, Nanchang.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 May;13(2):177-80.
The effect of 15-Mt-PGF2 alpha on CCl4-induced injury of primary cultured hepatocytes was studied. 15-Mt-PGF2 alpha treatment (2 mg/L) significantly decreased CCl4 (10 mmol/L)-induced damages of primary cultured rat heptocytes as indicated by decreases GPT and GOT leakage and LPO production. 15-Mt-PGF2 alpha significantly promoted 3H-uridine incorporation into RNA and [3H]-thymidine incorporation into DNA of the rat hepatocytes. Cytopathology study showed that 15-Mt-PGF2 alpha attenuated damages of mitochondria, endoplasmic reticulum and ribosome caused by CCl4. 15-Mt-PGF2 alpha appeared to maintain the stability of rat hepatocytes by inhibiting lipid peroxidation. These results indicated that 15-Mt-PGF2 alpha has notable protective effect on primary cultured rat hepatocytes against CCl4-induced damage by reducing lipid peroxidation and promoting synthesis of RNA and DNA.
研究了15-甲基前列腺素F2α对四氯化碳诱导的原代培养肝细胞损伤的影响。15-甲基前列腺素F2α处理（2mg/L）显著降低了四氯化碳（10mmol/L）诱导的原代培养大鼠肝细胞损伤，表现为谷丙转氨酶（GPT）和谷草转氨酶（GOT）漏出以及脂质过氧化物（LPO）生成减少。15-甲基前列腺素F2α显著促进3H-尿苷掺入大鼠肝细胞的RNA以及[3H]-胸腺嘧啶掺入DNA。细胞病理学研究表明，15-甲基前列腺素F2α减轻了四氯化碳引起的线粒体、内质网和核糖体损伤。15-甲基前列腺素F2α似乎通过抑制脂质过氧化来维持大鼠肝细胞的稳定性。这些结果表明，15-甲基前列腺素F2α通过减少脂质过氧化和促进RNA及DNA合成，对四氯化碳诱导的原代培养大鼠肝细胞损伤具有显著的保护作用。
