Effects of s-adenosylmethionine on methionine metabolism and lipid peroxidation of liver from rats with ethanol-induced liver injury
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摘要: 观察腺苷蛋氨酸(S-adenosylmethionine,SAM)对酒精性肝损伤大鼠的防治作用及机制。48只SD大鼠随机分为4组(每组12只):正常对照组、模型组、腺苷蛋氨酸低及高剂量组。除对照组外,其余三组给予酒精、鱼油灌胃配合高脂饮食构建酒精性肝损伤大鼠模型,造模4周后腹腔注射SAM,第8周处死全部大鼠。测定血浆总同型半胱氨酸(total plasm a homocysteine,tHcy)、血清丙氨酸转移酶(ALT)、甘油三酯(TC)、总胆固醇(TG)、肿瘤坏死因子-α(TNF-α)、转化生长因子(TGF-β)水平、肝匀浆丙二醛(MDA)和还原型谷胱甘肽(GSH)含量,及肝组织病理学检测。与对照组比较,模型组大鼠tHcy、ALT、TC、TG、TNF-α、TGF-β、MDA含量均明显升高(P<0.01);GSH水平降低(P<0.01)。与模型组比较,SAM治疗组ALT、TC、TG、MDA(P<0.01)和TNF-α、TGF-β明显降低(P<0.05),GSH含量升高(P<0.01),但血浆tHcy水平无显著变化(P>0.05)。SAM低、高剂量组...Abstract: To investigate the effects of S-adenosylmethionine (SAM) on ethanol-induced liver injury in rats.48 female SD rats were randomly divided into 4 groups, control, model, low dose and high dose SAM groups.Except control group, all rats were fed with high fat-containing diet plus ethanol and fish oil gavage for 8 weeks.SAM were administered by intraperitioneal injection after 4 weeks exposure of ethanol.Plasma total homocysteine (tHcy) , serum aminotransferase activity (ALT) , total cholesterol (TC) , triglyceride (TG) , TNF-α, TGF-β level, and liver malondialdehyde (MDA) , and glutathione (GSH) contents were assayed, Liver histology was also examined.Compared with control group, model group rats developed markedly liver damage, accompanied with an increased level of tHcy, ALT, TC, TG, TNF-α, TGF-β and MDA, and decreased level of GSH (P<0.01) .In treatment groups, SAM significantly protected from liver injury, reduced ALT, TC, TG, MDA, TNF-α and TGF-β levels (P<0.05) , and enhandced GSH level (p<0.01) .But plasma tHcy levels was not affected significantly (P>0.05) .there was no statistical difference in above parameters between the two dose groups (P>0.05) .SAM prevents liver from alcohol-induced injury in rats by reducing liver lipid peroxidation, anti-inflammation and anti-hyperplasia.SAM does not affect the plasma tHcy level.
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Key words:
- alcohol-induced liver injury /
- S-adenosyolethionine /
- lipid peroxidation /
- TNF-α /
- TGF-β
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