Zamin Idilio, Mattos Angelo Alves de, Mattos Angelo Zambam de, Coral Gabriela, Santos Diogo, Rhoden Cláudia
Post-Graduation Program in Hepatology, Fundação Faculdade Federal de Ciências Médicas de Porto Alegre, Porto Alegre, RS, Brazil.
Arq Gastroenterol. 2010 Jan-Mar;47(1):86-92. doi: 10.1590/s0004-28032010000100015.
No effective treatment is available for nonalcoholic steatohepatitis in nowadays.
To develop a model of nonalcoholic steatohepatitis induced by a methionine and choline deficient diet, as well as to evaluate the role of metformin, vitamin E and simvastatin in the nonalcoholic steatohepatitis progression.
The study analyzed prospectively 50 Wistar rats for a 90-day period and divided them into five groups of 10 rats. One group was given standard rat diet and the others received the methionine and choline deficient diet. Among the four groups that received this diet, one received saline 0,9% and the others received metformin, vitamin E or simvastatin. After the study period, the animals were sacrificed and their blood was collected for biochemical analysis. The livers were removed for lipoperoxidation analysis and for the histological examinations.
The methionine and choline deficient diet was able to induce steatosis in 100% of the animals and nonalcoholic steatohepatitis in 27 (69.2%). The alanine aminotransferase levels were significantly higher in the simvastatin group. The aspartate aminotransferase levels were also higher in the simvastatin group, but were statistically significant only in relation to the standard diet group. When lipoperoxidation values were compared, the groups that received standard rat diet and methionine and choline deficient with vitamin E presented significantly lower rates than the others. The presence of fibrosis was significantly smaller in the group receiving vitamin E.
The diet used was able to induce steatosis and nonalcoholic steatohepatitis. Besides vitamin E showed to reduce the liver oxidative stress, as well as the fibrosis development.
目前尚无有效的非酒精性脂肪性肝炎治疗方法。
建立蛋氨酸和胆碱缺乏饮食诱导的非酒精性脂肪性肝炎模型，并评估二甲双胍、维生素E和辛伐他汀在非酒精性脂肪性肝炎进展中的作用。
本研究对50只Wistar大鼠进行了为期90天的前瞻性分析，并将它们分为五组，每组10只。一组给予标准大鼠饮食，其他组给予蛋氨酸和胆碱缺乏饮食。在接受这种饮食的四组中，一组接受0.9%生理盐水，其他组分别接受二甲双胍、维生素E或辛伐他汀。研究期结束后，处死动物并采集血液进行生化分析。取出肝脏进行脂质过氧化分析和组织学检查。
蛋氨酸和胆碱缺乏饮食能够使100%的动物发生脂肪变性，27只（69.2%）发生非酒精性脂肪性肝炎。辛伐他汀组的丙氨酸氨基转移酶水平显著更高。辛伐他汀组的天冬氨酸氨基转移酶水平也更高，但仅与标准饮食组相比有统计学意义。比较脂质过氧化值时，接受标准大鼠饮食和蛋氨酸和胆碱缺乏饮食加维生素E的组的发生率明显低于其他组。接受维生素E的组纤维化的发生率明显更低。
所用饮食能够诱导脂肪变性和非酒精性脂肪性肝炎。此外，维生素E显示出可减轻肝脏氧化应激以及纤维化的发展。
