Salvianolic acid A attenuates CCl
| Autor: | Rong, Wang, Fuxing, Song, Shengnan, Li, Bin, Wu, Yanqiu, Gu, Yongfang, Yuan |
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| Rok vydání: | 2018 |
| Předmět: |
Liver Cirrhosis
Male Caspase 3 TOR Serine-Threonine Kinases AKT/mTOR salvianolic acid A Rats Rats Sprague-Dawley Phosphatidylinositol 3-Kinases Caffeic Acids Lactates Animals Enzyme Inhibitors Carbon Tetrachloride Proto-Oncogene Proteins c-akt Signal Transduction bcl-2-Associated X Protein Original Research liver fibrosis Bcl-2/Bax caspase-3/cleaved caspase-3 |
| Zdroj: | Drug Design, Development and Therapy |
| ISSN: | 1177-8881 |
| Popis: | Background: Liver fibrosis occurs due to chronic liver disease due to multiple pathophysiological causes. The main causes for this condition are chronic alcohol abuse, nonalcoholic steatohepatitis, and infection due to hepatitis C virus. Currently, there is more and more information available about the molecular as well as cellular mechanisms, which play a role in the advancement of liver fibrosis. However, there is still no effective therapy against it. Purpose: In order to find an effective treatment against liver fibrosis, our study explored whether salvianolic acid A (SA-A), a traditional Chinese medicine extracted from the plant Danshen, could effectively inhibit the liver fibrosis, which is induced by CCl4 in vivo. Methods: The effects of SA-A were evaluated by assessing the parameters related to liver fibrosis such as body weight, histological changes, and biochemical parameters. Thereafter, the related protein or gene levels of P13K/AKT/mTOR, Bcl-2/Bax and caspase-3/cleaved caspase-3 signaling pathways were determined by western blotting, real-time PCR or immunohistochemistry staining. Results: According to the results of our study, SA-A could reduce liver fibrosis by inhibiting liver function, liver fibrosis index, collagen deposition, and improving the degree of liver fibrosis in rats. Mechanistically, the PI3K/AKT/mTOR signaling cascade was inhibited by SA-A to prevent the stimulation of hepatic stellate cell, as well as the synthesis of extracellular matrix, and regulated Bcl-2/Bax and caspase-3/cleaved caspase-3 signaling pathways to prevent hepatocyte apoptosis. Conclusion: The novel findings of this study suggested that SA-A could reduce liver fibrosis and the molecular mechanisms behind it are closely associated with the regulation of PI3K/AKT/mTOR, Bcl-2/Bax and caspase-3/cleaved caspase-3 signaling pathways. |
| Databáze: | OpenAIRE |
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