摘要
目的探讨氧应激和脂质过氧化在高脂饮食所致脂肪性肝炎形成中的作用。方法雄性SD大鼠30只随机分为3组,每组10只。正常组普通饲料喂养;模型Ⅰ、Ⅱ组喂高脂饲料;12周末处死正常组、模型Ⅰ组大鼠;模型Ⅱ组大鼠继续喂养至16周末处死,测定血清转氨酶(ALT、AST),全血谷胱甘肽过氧化物酶(GSH-PX),肝匀浆丙二醛(MDA)含量,超氧化物歧化酶(SOD)活性,总抗氧化能力(T-AOC),一氧化氮(NO),诱导型一氧化氮合酶(iNOS),谷胱甘肽(GSH)水平,观察肝组织学改变。结果模型组大鼠12周出现单纯性脂肪肝,16周发展为脂肪性肝炎。与正常组比,模型组大鼠肝组织脂质过氧化产物MDA含量明显增多,而抗氧化物SOD,GSH,GSH-PX含量明显降低,且肝脏的脂肪变性严重程度随着高脂饮食喂养的时间延长而加剧。结论氧应激和脂质过氧化在肝组织脂肪变性后炎症的过程中发挥重要作用。
Objective To explore the role of oxygen stress and lipid peroxidation in tbe establishment of stcatnhepatitis in rats fed by hlgh-fat diets. Methods Thlny male. Sprague Dawlcy rats were assigned into three groups （ n = 10） at random. The rats fed by normal foods served as controls. The rats in model groups （ I , II ） wire fed with high - fat diets. The animals in control group and model I group were killed at the end of the 12th week, and the ones left were killed at the end of the 16th week. Blood samples were collected for the detection of serum aspartate transaminasc （AST） , alanine aminotransferase （ALT） and glutathione peroxi- dase （GSH-PX） , and liver tissues were obtained for the detection of malondialdehyde （MDA） contents, superoxlde dismutase （SOD） activity, total antioxidative capacity （T-AOC） , and nitric oxide （NO） , inducible nitric oxide synthase （iNOS） and glutathione （GSH） levels. The histological changes were observed under light microscope. Results Pure fatty liver was formed in the model rats after in the 12th week, and fatty hepatitis was established in the 16th week. In comparison with those of normal rats, the contents of MDA were increased （ P 〈 0.01 ） but anti-oxide SOD, GSH, GSH-PX contents were decreased significantly （ P 〈 0.05, or P 〈 0.01 ）. The severity of hepatic fatty degeneration aggravated with the prolonging of the high-fat diets taking duration. Conclusion Oxidative stress and lipid peroxidation may play an important role in the formation of liver inflammation eell infiltration.
出处
《临床军医杂志》
CAS
2007年第5期677-679,共3页
Clinical Journal of Medical Officers
关键词
氧应激
脂质过氧化
非酒精性脂肪性肝炎
oxygen stress
lipid peroxidation
nonalcoholic steatohepatitis
