腺苷蛋氨酸对酒精性脂肪肝大鼠治疗效果及机制的研究

目的观察腺苷蛋氨酸(SAM)对酒精性肝损伤的防治作用及机制。方法将48只SD大鼠随机分为对照组(Ⅰ组)、模型组(Ⅱ组)及SAM低剂量组(Ⅲ组)、SAM高剂量组(Ⅳ组),每组12只。除对照组外,其余三组给予酒精、鱼油灌胃配合高脂饮食诱导酒精性肝损伤,4周后Ⅰ、Ⅱ组腹腔注射生理盐水,Ⅲ、Ⅳ组分别腹腔注射SAM100mg/kg、200mg/kg,第8周均处死。测定血浆总同型半胱氨酸(tHcy)浓度、血清丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)浓度;测定肝匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)含量,行肝脏病理组织学检查。结果与Ⅰ组比较,Ⅱ组肝损伤明显,表现为ALT、ASTt、Hcy水平升高,肝脂肪变性,MDA含量增加,SOD和GSH水平下降;Ⅲ、Ⅳ组MDA降低、GSH升高,但tHcy水平和肝组织SOD含量无显著变化,Ⅲ、Ⅳ组间无明显差别。结论SAM可防治大鼠酒精性肝损伤,其机制可能与调节肝脏内氧化抗氧化系统的平衡有关;SAM对血浆tHcy水平无明显影响。

Objective： To investigate the effects of S-adenosylmethionine （SAM） on ethanol-induced liver injury in rats. Methods ： 48 female SD rats were randomly divided into control group（ Ⅰ group）, model group（ Ⅱ group）, SAM low dose group（ Ⅲ group）, SAM high dose group（ Ⅳ group）. Except control group, all rats were fed high fat-containing diet plus ethanol and fish oil gavage for 8 weeks. After 4 weeks exposure of ethanol Ⅱ , Ⅳ groups with 100mg/kg, 200mg/kg SAM intraperitioneal injection respectively; Ⅰ , Ⅱ groups with Sodium Chloride. Plasma total homocysteine, serum aminotransferase activity, and liver malondialdehyde （MDA）, superoxidezed dismutase （SOD） and glutathione （GSH） contentswere assayed, laver histology was also examined. Results： Compared with Ⅰ group, Ⅱ group rats developed markedly liver damage, evidenced by an increase in serum ALT ,AST, tHcy levels, and pronounced fatty liver. The liver injury was accompanied by elevated MDA contents and decreasedSOD and GSH levels . However, Ⅲ , Ⅳ groups treatment significantly protected the liver injury , reduced the MDA contents, and enhanced the GSH levels, but Plasma total homocysteine levels and liver SOD levels were not affected significantly . There was no difference in the above parameters between the two dose groups. Conclusions： SAM prevents ethanol-induced liver injury in rats by modulating the oxidant and antioxidant system in the liver, SAM does not affect the plasma total homocysteine levels.