...
首页> 外文期刊>World Journal of Gastroenterology >Effect of lactulose on establishment of a rat non-alcoholic steatohepatitis model.
【24h】

Effect of lactulose on establishment of a rat non-alcoholic steatohepatitis model.

机译:乳果糖对大鼠非酒精性脂肪性肝炎模型建立的影响。

获取原文
获取原文并翻译 | 示例
           

摘要

AIM: To explore the relationship between changes of intestinal environment and pathogenesis of non-alcoholic steatohepatitis (NASH). METHODS: Forty-two Sprague-Dawley rats were randomly divided into model group (n = 24), treatment group (n = 12), and control group (n = 6). The rats of model and treatment groups were given high-fat diet, and those of the control group were given normal diet. Furthermore, the rats of treatment group were given lactulose after 8 wk of high-fat diet. Twelve rats of the model group were killed at 8 wk of high-fat diet. At the 16 wk the rats of treatment group, control group, and the rest of the model group were killed. The serum levels of aminotransferase were measured and the histology of livers was observed by H and E staining. RESULTS: The livers of rats presented the pathological features of steatohepatitis with higher serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the model group after 16 wk. Compared to the model group, the serum levels of ALT and AST in treatment group decreased significantly and were close to the normal group, and the hepatic inflammation scores also decreased markedly than those in the model group after 16 wk (5.83+/-2.02 vs 3.63+/-0.64, P<0.05), but were still higher than those in the model group after 8 wk (3.63+/-0.64 vs 1.98+/-0.90, P<0.05). However, the degree of hepatic steatosis had no changes in treatment group compared to the model group after 16 wk. CONCLUSION: Lactulose could ameliorate the hepatic inflammation of rats with steatohepatitis induced by fat-rich diet, but could not completely prevent the development of steatohepatitis. It is suggested that intestinal environmental changes such as intestinal bacteria overgrowth, are one of the important factors in the pathogenesis of NASH.
机译:目的:探讨肠道环境变化与非酒精性脂肪性肝炎(NASH)发病机制的关系。方法:42只Sprague-Dawley大鼠随机分为模型组(n = 24),治疗组(n = 12)和对照组(n = 6)。模型组和治疗组大鼠均采用高脂饮食,对照组为正常饮食。此外,高脂饮食8周后给予治疗组大鼠乳果糖。模型组的12只大鼠在8周高脂饮食时被处死。在第16周,处死治疗组,对照组和模型组的其余部分。测定血清中的氨基转移酶水平,并通过H和E染色观察肝脏的组织学。结果:模型组16周后,大鼠肝脏表现为脂肪性肝炎的病理特征,血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)较高。与模型组相比,治疗组的血清ALT和AST水平显着下降,接近正常组,且16 wk后肝炎评分也明显低于模型组(5.83 +/- 2.02 vs. 3.63 +/- 0.64,P <0.05),但仍高于模型组在8周后(3.63 +/- 0.64对1.98 +/- 0.90,P <0.05)。然而,与模型组相比,治疗组在16周后肝脂肪变性程度没有变化。结论:乳果糖可减轻高脂饮食引起的脂肪性肝炎大鼠的肝炎,但不能完全预防脂肪性肝炎的发展。提示肠道环境变化,例如肠道细菌过度生长,是NASH发病机理的重要因素之一。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号