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Open AccessArticle

Comprehensive Study of Multiple Stages Progressing to Nonalcoholic Steatohepatitis with Subsequent Fibrosis in SD Rats

by Lulu Wang 1,2, Susu Wu 1,2, Minxuan Cai 1,2, Ji Ma 1,2, Shengcun Li 1,2, Maoru Li 1,2, Yan Xu 1,2, Lixin Wei 3,4 and Jing Shang 1,2,3,4,*
1
State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China
2
Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing 211198, China
3
Key Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining 810008, China
4
Qinghai Key Laboratory of Tibetan Medicine Pharmacology and Safety Evaluation, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining 810008, China
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2017, 18(8), 1681; https://doi.org/10.3390/ijms18081681
Received: 29 June 2017 / Revised: 17 July 2017 / Accepted: 17 July 2017 / Published: 18 August 2017
(This article belongs to the Section Biochemistry)
Because of the absence of the time course of histological nonalcoholic fatty hepatitis with subsequent fibrotic progression, the effective approaches available for controlling the onset and progression of non-alcoholic steatohepatitis (NASH) remain limited. Therefore, we detected the serum and liver tissue related lipid metabolism disorder, liver pathology and relative molecular makers alteration dynamically in a high fat-sucrose diet during different time points. High fat-sucrose diet significantly increased the serum lipid level on day 10. The excess lipid accumulation in liver was referred to as simple steatosis after the feeding of a high fat-sucrose diet for 20 days. The high fat-sucrose diet induced a hepatic inflammation response on day 30. Similarly, hepatic fibrosis was also initiated on day 30 and gradually formed from the 30th to the 50th day. Oxidative stress may be related with the process from NASH to liver fibrosis. Insulin resistance was involved in the progression from hepatic steatosis to NASH with hepatic fibrosis from the 20th to the 50th day. In conclusion, we established a high fat-sucrose diet induced nonalcoholic fatty hepatitis with liver fibrosis rat model, which presented the time course of histological nonalcoholic steatohepatitis and the initiation and progression change of characteristic molecular makers in the process from steatosis to hepatic fibrosis. View Full-Text
Keywords: nonalcoholic steatohepatitis; liver fibrosis; lipid metabolism; chronic inflammation; oxidative stress; insulin resistance nonalcoholic steatohepatitis; liver fibrosis; lipid metabolism; chronic inflammation; oxidative stress; insulin resistance
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MDPI and ACS Style

Wang, L.; Wu, S.; Cai, M.; Ma, J.; Li, S.; Li, M.; Xu, Y.; Wei, L.; Shang, J. Comprehensive Study of Multiple Stages Progressing to Nonalcoholic Steatohepatitis with Subsequent Fibrosis in SD Rats. Int. J. Mol. Sci. 2017, 18, 1681.

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