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Lan Zhong

Publications and source records attributed to Lan Zhong.

5 recordsLinked to original sources

Effects of ursodeoxycholic acid and/or low-calorie diet on steatohepatitis in rats with obesity and hyperlipidemia.

AIM: To evaluate the effects of ursodeoxycholic acid (UDCA) and/or low-calorie diet (LCD) on a rat model of nonalcoholic steatohepatitis (NASH). METHODS: Fifty-five Sprague-Dawley rats were divided into five groups. The control group (n = 9) was fed with standard rat diet for 12 wk, NASH group (n = 10) was fed with high-fat diet consisted of normal diet, 10% lard oil and 2% cholesterol for 12 wk, UDCA group (n = 10) was fed with high-fat diet supplemented with UDCA at a dose of 25 mg/(kg.d) in drinking water for 12 wk, LCD group (n = 10) was fed with high-fat diet for 10 wk and then LCD for 2 wk, and UDCA+LCD group (n = 15) was fed with high-fat diet for 10 wk, followed by LCD+UDCA for 2 wk. At the end of the experiment, body weight, serum biochemical index, and hepatopathologic changes were examined. RESULTS: Compared with the control group, rats in the NASH group had significantly increased body weight, liver weight, and serum lipid and aminotransferase levels. All rats in the NASH group developed steatohepatitis, as determined by their liver histology. Compared with the NASH group, there were no significant changes in body weight, liver weight, blood biochemical index, the degree of hepatic steatosis, and histological activity index (HAI) score in the UDCA group; however, body and liver weights were significantly decreased, and the degree of steatosis was markedly improved in rats of both the LCD group and the UDCA+LCD group, but significant improvement with regard to serum lipid variables and hepatic inflammatory changes were seen only in rats of the UDCA+LCD group, and not in the LCD group. CONCLUSION: LCD might play a role in the treatment of obesity and hepatic steatosis in rats, but it exerts no significant effect on both serum lipid disorders and hepatic inflammatory changes. UDCA may enhance the therapeutic effects of LCD on steatohepatitis accompanied by obesity and hyperlipidemia. However, UDCA alone is not effective in the prevention of steatohepatitis induced by high-fat diet.

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A statistical approach designed for finding mathematically defined repeats in shotgun data and determining the length distribution of clone-inserts.

The large amount of repeats, especially high copy repeats, in the genomes of higher animals and plants makes whole genome assembly (WGA) quite difficult. In order to solve this problem, we tried to identify repeats and mask them prior to assembly even at the stage of genome survey. It is known that repeats of different copy number have different probabilities of appearance in shotgun data, so based on this principle, we constructed a statistical model and inferred criteria for mathematically defined repeats (MDRs) at different shotgun coverages. According to these criteria, we developed software MDRmasker to identify and mask MDRs in shotgun data. With repeats masked prior to assembly, the speed of assembly was increased with lower error probability. In addition, clone-insert size affect the accuracy of repeat assembly and scaffold construction, we also designed length distribution of clone-inserts using our model. In our simulated genomes of human and rice, the length distribution of repeats is different, so their optimal length distributions of clone-inserts were not the same. Thus with optimal length distribution of clone-inserts, a given genome could be assembled better at lower coverage.

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Effects of low-calorie diet on steatohepatitis in rats with obesity and hyperlipidemia.

AIM: To evaluate the effects of low calorie diet (LCD) on nonalcoholic steatohepatitis (NASH) in rats with obesity and hyperlipidemia. METHODS: 29 Sprague-Dawley (SD) rats were randomly divided into three groups. The animals in control (n=9) and NASH group (n=10) were fed on standard rat diet and high fat diet respectively for 12 weeks, ten rats in LCD group were fed on high fat diet for 10 weeks and then low calorie diet for 2 weeks. At the end of the experiment, body weight, abdominal adipose content, liver function, and hepatopathological changes were examined to evaluate the effect of different feeding protocols on the experimental animals. RESULTS: There was no death of animal in the experimental period. All rats in the NASH group developed steatohepatitis according to liver histological findings. Compared with the control group, body weight (423.5+/-65.2 vs 351.1+/-43.0 g, P<0.05), abdominal adipose content (14.25+/-1.86 vs 9.54+/-1.43, P<0.05), liver index (3.784+/-0.533 vs 2.957+/-0.301 %, P<0.01), total serum cholesterol (1.60+/-0.41 vs 1.27+/-0.17 mmol/L,P<0.05) and free fatty acids (728.2+/-178.5 vs 429.2+/-96.7 mmol/L, P<0.01), serum alanine aminotransferase (1,257.51+/-671.34 vs 671.34+/-118.57 nkat/L, P<0.05) and aspartic aminotransferase (2,760.51+/-998.66 vs 1,648.29+/-414.16 nkat/L, P<0.01) were significantly increased in the NASH group. Whereas, when rats were fed on LCD protocol, their body weight (329.5+/-38.4 g, P<0.01), abdominal adipose content (310.21+/-1.52 g, P<0.05), liver index (3.199+/-0.552 %, P<0.05), and serum alanine aminotransferase (683.03+/-245.49 nkat/L, P<0.05) were significantly decreased, and the degree of hepatic steatosis (P<0.05) was markedly improved compared with those in the NASH group. However, no significant difference was found in serum lipid variables and hepatic inflammatory changes between the two groups. CONCLUSION: LCD might play a role in the prevention and treatment of obesity and hepatic steatosis in SD rats, but it exerts no significant effects on both serum lipid disorders and hepatic inflammatory changes.

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[Dynamic expression of tenascin in rat liver during liver fibrogenesis induced by CCl(4)].

OBJECTIVE: To study the expression of tenascin in normal and fibrotic rat liver. METHODS: Liver fibrosis induced in rat with CCl(4) were divided into three stages: the stage of hepatic injury (4 weeks), early stage of hepatic fibrosis (8 weeks) and later stage of hepatic fibrosis (12 weeks). Tenascin expression in liver tissue was observed by immunohistochemical method and in situ hybridization using digoxigenin-labelled DNA probe. RESULTS: In normal rat liver there was a weak staining for tenascin. In both liver injury stage and early stage of hepatic fibrosis, both mRNA signal and immunostaining for tenascin were significantly increased as compared to that in normal liver. In later stage of hepatic fibrosis, mRNA signal and immunostaining for tenascin were decreased compared with that in early stage of hepatic fibrosis. The cellular source of tenascin in liver mainly restricted in mesenchymal cells. CONCLUSIONS: Tenascin is a component of the extracellular matrix of liver tissue. Plays a role in early matrix organization during liver fibrogenesis.

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[Influence of ursodeoxycholic acid on the therapeutic effects of low-calorie diet in obesity and hyperlipidemia rats with steatohepatitis].

OBJECTIVE: To explore the influence of ursodeoxycholic acid on the therapeutic effects of low-calorie diet in steatohepatitis with obesity and hyperlipidemia. METHODS: Thirty-five Sprague-Dawley rats fed with high-fat diet for 10 weeks were randomly allocated into 3 groups, and continued to experiment for 2 weeks. The animals in model group (n = 10) were still fed with high-fat diet; low-calorie diet group (n = 10) with common diet but only one third of the amount of normal demand; ursodeoxycholic acid group (n = 15) with low-calorie diet and ursodeoxycholic acid (15 mg/kg.d(-1)); and another 9 rats with common diet for 12 weeks as normal group. RESULTS: Compared with normal group, such indexes as body weight, liver weight, and the level of serum lipids and aminotransferase were all increased significantly in model group. Furthermore, all rats in model group developed steatohepatitis. On the other hand, such indexes as body weight and the degree of steatosis in rats of low-calorie diet group were decreased sharply compared with those in model group, but neither disorders of serum lipid nor the degree of hepatic inflammation and necrosis in low-calorie diet group were improved obviously. Disorders of serum lipid, aspartate aminotransferase, hepatic inflammation and necrosis in ursodeoxycholic acid group were ameliorated to some extent. CONCLUSIONS: Ursodeoxycholic acid might help to improve the therapeutic effects of low-calorie diet on steatohepatitis with obesity and hyperlipidemia.

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