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目的：研究还原型谷胱甘肽（ＧＳＨ）对化学致癌原Ｎ－二乙基亚硝胺（ＤＥＮ）诱致雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠肝癌的保护作用。方法：雄性 ＳＤ大鼠 ７５只分成 ７组，每天 ＤＥＮ ８ｍｇ／ｋｇ ｉ．ｇ 诱发大鼠肝癌模型，分别不同途径预防性给予ＧＳＨ。结果：对照组１６ｗ后大鼠的肝脏癌变率为７６．５％，伴有镜检典型的弥漫性癌结节、畸型核分裂和重度肝硬化及胆管炎，于 １２ｗ及 １６ｗ ＡＫＰ及 γ－ＧＴ明显增高；同剂量 ＤＥＮ １６ｗ伴以 ＧＳＨ １５０ｍｇ／ｋｇ、３００ｍｇ／ｋｇ、 １０００ｍｇ／ｋ（ｉｐ）及 １０００ｍｇ／ｋｇ（ ｉｇ） １６ｗ，明显降低癌变率，分别降为１１．１％、１６．７％、１６．７％及１８．２％；ＧＳＨ大剂量组大鼠未癌变，肝组织仅见少量纤维增生，ＡＫＴ及γ－ＧＴ值与正常大鼠无显著差异；ＤＥＮ诱癌１２ｗ后用ＧＳＨ治疗４ｗ对大鼠肝脏癌变率无明显防治效果。结论：早期用外源性 ＧＳＨ对 ＤＥＮ诱发大鼠肝癌有预防作用，ＤＥＮ诱发肝癌形成后用ＣＳＨ无效。
AIM: To investigate the protective effects of reduced glutathione (GSH) on hepatocarcinoma induced by chemically induced N-diethylnitrosamine (DEN) in male Sprague-Dawley rats. Methods: Seventy-five male Sprague-Dawley rats were divided into 7 groups with DEN 8 mg / kg daily. g induced rat liver cancer model, respectively, different ways of preventive administration of GSH. Results: The liver canceration rate of rats in control group was 76.5% after 16 weeks, with typical diffuse cancerous nodules, degenerative mitosis and severe cirrhosis and cholangitis, and obvious AKP and γ-GT on 12th and 16th weeks (P <0.05). The same dose of DEN 16w with GSH 150mg / kg, 300mg / kg, 1000mg / kg and 1000mg / kg 16w significantly reduced the canceration rate to 11.1% and 16.7% 16.7% and 18.2%, respectively. GSH high-dose group had no carcinogenesis, only a small amount of fibrosis in liver tissue, no significant difference in AKT and γ-GT values with normal rats. There was no obvious prevention and cure effect on rat liver cancer rate. CONCLUSION: Exogenous GSH can prevent DEN-induced hepatocarcinogenesis in rats and D-induced hepatocarcinogenesis after CSH is ineffective.