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| Study of anti-liver fibrosis effect of astralosides via circular RNA34116 |
| ZHOU Yuping1, YANG Ping2, TANG Chunlan3, QU Hui1, LYU Xueyou1, HU Guimei1 |
| 1.Department of Gastroenterology, the Affiliated Hospital of Medical School of Ningbo University, Ningbo 315020, China; 2.School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China; 3.Department of Preventive Medicine, Medical School of Ningbo University, Ningbo 315211, China |
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ZHOU Yuping,YANG Ping,TANG Chunlan, et al. Study of anti-liver fibrosis effect of astralosides via circular RNA34116[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2019, 49(4): 263-266.
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Abstract Objective: To study the mechanism underlying Astragalosides in the inhibition of hepatic fibrosis via circularRNA. Methods: Mice were randomly divided as normal group, CCl4 model group, Astragalosides group and sorafenib group, with 8 mice in each group. A CCl4 liver fibrosis model was established. After drug intervention with Astragalosides, the serum ALT and TBIL, pathological changes (HE staining and Masson staining) of the liver and relative mmu_circ_34116 expressionwere detected and observed by RT-PCR. Results: Histopathological results showed that, compared with the normal group, liver tissue inflammation and collagen deposition were significantly increased Astragalosides and sorafenib significantly reduced inflammation and collagen deposition. The results of serum liver function showed that Astragalosides and sorafenib significantly reduced the level of ALT and TBIL after intervention in the model mice. RT-PCR results showed that, compared with the normal group, the expression of mmu_circ_34116 in liver tissue was significantly reduced in CCl4 model group, and its expression was significantly increased after intervention with Astragalosides in the model, but sorafenib had no significant effect on its expression. Conclusion: Astragalosides significantly inhibited the development of liver fibrosis. The mechanism may be associated with over expression of mmu_circ_34116.
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Received: 01 November 2018
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