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作 者:吴斌[1] 王崇文[1] 徐家瑞[1] 祝金泉 徐宜宜[1]
机构地区:[1]江西医学院第一附属医院
出 处:《中国应用生理学杂志》1997年第2期177-180,共4页Chinese Journal of Applied Physiology
摘 要:采用大鼠离体肝细胞原代培养24h,并利用四氯化碳CCl4造成急性肝细胞损伤模型,检定15-甲基-前列腺素F2α(15-Mt-PGF2α)对肝细胞损伤的影响。结果表明:(1)15-Mt-PGF2α可显著降低中毒肝细胞脂质过氧化物水平,抑制肝细胞脂质过氧化,并降低谷丙转氨酶(GPT)和谷草转氨酶(GOT)水平,稳定脂质膜。(2)显著促进中毒肝细胞RNA和DNA的合成。(3)超微结构证实15-Mt-PGF2α能减轻CCl4对肝细胞脂质膜,染色质,线粒体,内质网和核蛋白体的损害。The effect of 15 Mt PGF 2α on CCl 4 induced injury of primary cultured hepatocytes was studied. 15 Mt PGF 2α treatment (2mg/L) significantly decreased CCl 4 (10mmol/L) induced damages of primary cultured rat heptocytes as indicated by decreases GPT and GOT leakage and LPO production. 15 Mt PGF 2α significantly promoted 3 H uridine incorporatin into RNA and thymidine incorporation into DNA of the rat hepatocytes. Cytopathology study showed that 15 Mt PGF 2α attenuated damages of mitochondria, endoplasmic reticulum and ribosome caused by CCl 4. 15 Mt PGF 2α appeared to maintain the stability of rat hepatocytes by inhibiting lipid peroxidation. These results indicated that 15 Mt PGF 2α has notable protective effect on primary cultured rat hepatocytes against CCl 4 induced damage by reducing lipid peroxidation and promoting synthesis of RNA and DNA.
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