The Restorative Effect of Taurine on Experimental Nonalcoholic Steatohepatitis

Abstract

Our objective was to explore the restorative effect of taurine on experimental nonalcoholic steatohepatitis (NASH). Thirty-six SD rats were randomly divided into three groups, 12 in each group: the normal group was fed standard rat diet; the model group and the treatment group were both fed a high-fat rat diet for 12 weeks, and the rats in the treatment group were simultaneously injected with taurine subcutaneously for 8 weeks. Hepatic histological change was observed; TNF-alpha and TGF-beta(1) protein expression was identified by immunohistochemistry; mRNA expression of TNF-alpha, TGF-beta(1), type I procollagen, and adiponectin was measured by RT-PCR; body weight, weight gain, liver weight, and liver index were measured; and biochemical parameters monitored included serum transaminases, serum lipids, fasting plasma glucose, and hepatic level of oxidative stress. Rats in the model group showed a significant increase in liver weight, liver index, serum transaminase activities, serum triglyceride, fasting plasma glucose, and oxidative stress; the mRNA expression of TNF-alpha, TGF-beta(1), and type I procollagen increased, whereas the expression of adiponectin decreased significantly, compared with that in the normal group. The typical hepatic lesions of NASH were observed histologically in the model group. Taurine treatment resulted in a significant decrease in liver weight, liver index, serum transaminase activities, serum triglyceride, fasting plasma glucose, and oxidative stress; the mRNA expression of TNF-alpha, TGF-beta(1), and type I procollagen decreased, but the expression of adiponectin increased significantly, compared with that in the model group. Histological improvement was observed in the treatment group. In conclusion, taurine could inhibit lipid peroxidation, improve lipid and glucose metabolism, decrease synthesis of TNF-alpha and TGF-beta(1), promote synthesis of adiponectin, and have a restorative effect on experimental NASH.

Effects of a Long-Term High-Fat Diet and Switching from a High-Fat to Low-Fat, Standard Diet on Hepatic Fat Accumulation in Sprague-Dawley Rats

“…In the previous three reports, high-fat diet induced histologically confirmed NASH, but hepatic fibrosis was not observed in SD rats; these results maybe due to the relatively short-term feeding [9][10][11]. Chen et al [12] reported that high-fat diet successfully induced NASH with hepatic fibrosis in SD rats, but they investigated rats only from 6-7 weeks of age for 12 weeks. In contrast, Romestaing et al [8] reported that in Wistar rats high-fat diet from 3 weeks of age for 14 weeks did not induce hepatic steatosis and fibrosis.…”

“…However, periportal fibrosis may occur independently of zone 3 hepatocellular injuries in severely obese individuals because adipocytokines from visceral adipose tissue can directly drain into the portal vein [19]. Chen et al [12] also reported perisinusoidal and periportal fibrosis in SD rats fed a high-fat diet for 12 weeks. Our results were in line with these observations.…”

“…In SpragueDawley (SD) rats, several reports have demonstrated that a high-fat diet induced NASH [9][10][11][12]. Of these, three reports were the results of relatively short-term feeding periods (3 to 6 weeks), and in histopathological examinations, hepatic steatosis and lobular inflammation were evident, but obvious fibrosis was not [9][10][11].…”

“…Of these, three reports were the results of relatively short-term feeding periods (3 to 6 weeks), and in histopathological examinations, hepatic steatosis and lobular inflammation were evident, but obvious fibrosis was not [9][10][11]. In contrast, Chen et al [12] reported that SD rats were fed a high-fat diet for 12 weeks and that severe macro-to micro-vesicular steatosis, lobular inflammation, focal necrosis, perisinusoidal and periportal fibrosis, and severe hepatocyte ballooning were observed.…”

Biochemical and Pathophysiological Aspects of the Treatment of Hepatic Encephalopathy in Rats

“…After one week, ten rats from each previous group were taken to compare the alteration which occurred due to induction of hepatic encephalopathy in rats. [20] with a little modification by Xiao et al…”