Therapeutic Effect of Puerarin on Non-Alcoholic Rat Fatty Liver by Improving Leptin Signal Transduction through JAK2/STAT3 Pathways

2009 ◽  
Vol 37 (01) ◽  
pp. 69-83 ◽  
Author(s):  
Peiyong Zheng ◽  
Guang Ji ◽  
Zansong Ma ◽  
Tao Liu ◽  
Lianjun Xin ◽  
...  

In order to investigate the mechanism of the therapeutic effect of puerarin on non-alcoholic fatty liver disease, a non-alcoholic fatty disease male rat model was induced by a high fat diet, all rats were randomly divided into a blank group, model group, simavastatin group and puerarin group. After 4 weeks of drug treatment, the liver was slided to investigate pathological morphology. Elisa was used to measure the total cholesterol (TC), triglyeride (TG) in liver, and leptin content in serum. RT-PCR and Western blotting were employed to detect liver leptin mRNA receptor expression and P-JAK2, P-STAT3 expression levels in the liver respectively. The results showed that puerarin significantly decreased the TG, TC content in liver of the non-alcoholic fatty disease rats, ameliorated steatosis in liver, lowered liver inflammatory reaction, decreased leptin level in serum, and enhanced the expression of leptin receptor mRNA and P-JAK2/P-STAT3 level. All the results demonstrated that puerarin can exhibit therapeutic effect on non-alcoholic fatty liver disease by improving leptin signal transduction through JAK2/STAT3 pathways.

Phytomedicine ◽  
2021 ◽  
Vol 85 ◽  
pp. 153550
Author(s):  
Qiao-Ping Li ◽  
Yao-Xing Dou ◽  
Zi-Wei Huang ◽  
Han-Bin Chen ◽  
Yu-Cui Li ◽  
...  

2017 ◽  
Vol 10 (3) ◽  
pp. 226-236 ◽  
Author(s):  
Min You ◽  
Alvin Jogasuria ◽  
Kwangwon Lee ◽  
Jiashin Wu ◽  
Yanqiao Zhang ◽  
...  

2015 ◽  
Vol 61 (10/2015) ◽  
Author(s):  
Zhuang Xianghua ◽  
Sun Fudun ◽  
Li Liang ◽  
Jiang Dongqing ◽  
Li Xiaobo ◽  
...  

2020 ◽  
Author(s):  
B. Fatemeh Nobakht M. Gh ◽  
Masoud arabfard

Abstract Purpose: Non-alcoholic fatty liver disease (NAFLD) is the most preventable type of chronic liver disease worldwide and a risk factor for developing cirrhosis or hepatocellular carcinoma (HCC) if untreated. Although experts have performed lots of efforts to find the underlying mechanisms of NAFLD, it remains a challenge to recognize them. The aim of this study is to distinguish common gene signature and pathways in the human liver during NAFLD progression through the systems biology method.Methods: In this study, the three microarray datasets, GSE48452, GSE63067 and GSE89632, were selected from the NCBI GEO database to explore differentially expressed genes (DEGs) among healthy controls, simple steatosis and non-alcoholic steatohepatitis (NASH) patients. Furthermore, protein-protein interaction (PPI) networks and pathway enrichment analysis were used to detect common genes and biological pathways in different stages of NAFLD.Results: The current study was included 47 healthy subjects, 36 patients with simple steatosis and 46 NASH patients. Common high degree genes among all three sets were CHI3L1, GFBP2, NRG1, PEG10 and FADS2. The top five genes in the hepatic PPI networks of three datasets were STAT3, JUN, CANX, FN1 and MYC. Signal transduction, immune response, and anti-apoptosis were the most important biological pathways between healthy vs. NASH, while cell communication, signal transduction and immune response were three top biological pathways between healthy vs. simple steatosis. Also, the most eminent biological pathways between NASH vs. simple steatosis were metabolism and energy pathways. Conclusion: The present study represented the unique and shared key genes and pathways between different stages of NAFLD, which may facilitate the understanding of the NAFLD mechanism and identify potential therapeutic targets in this disease.


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