Effect of Corilagin on the miR-21/smad7/ERK signaling pathway in a schistosomiasis-induced hepatic fibrosis mouse model |
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| Institution: | 1. Department of Hepatology, Hubei Provincial Hospital of Chinese Medicine, Wuhan 430074, PR China;2. School of Clinical Medicine, Hubei University of Chinese Medicine, Wuhan 430060, PR China;3. Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, PR China;4. School of Life Science, Hubei University, Wuhan 430062, PR China;5. Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, PR China;6. School of Basic Medical Sciences, Guangxi University of Chinese Medicine, Nanning 530200, PR China;7. School of Clinical Medicine, Guangxi University of Chinese Medicine, Nanning 530007, PR China;8. Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, PR China;1. Key Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Shanghai, The People''s Republic of China;4. WHO Collaborating Center for Tropical Diseases, Shanghai, The People''s Republic of China;5. National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention, Shanghai, The People''s Republic of China;7. Federal University Lafia, Lafia, Nasarawa, Nigeria;8. Wolfson Wellcome Biomedical Laboratories, Life Sciences, The Natural History Museum, London, United Kingdom;9. Zhejiang Academy of Medical Sciences, Hangzhou, Zhejiang, The People''s Republic of China;1. Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark;2. Chemistry and Biochemistry Laboratory, School of Agriculture, Policy and Development, University of Reading, Reading, United Kingdom;3. Institute for Immunological Research, University of Cartagena, Cartagena, Colombia |
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| Abstract: | This study sought to investigate the anti-fibrotic effect of Corilagin via interference with the miR-21/smad7/ERK signaling pathway in a schistosomiasis-induced hepatic fibrosis mouse model. Mice were infected with Schistosoma japonicum cercaria to establish the mouse model of schistosomiasis-induced hepatic fibrosis. At four weeks after infection, the groups were given different medications. The living conditions were observed. Real-time PCR was employed to detect the mRNA levels of miR-21, smad7 and connective tissue growth factor (CTGF), and western blotting was used to examine the protein levels of smad7, CTGF, smad1, p-smad1, smad2, p-smad2, ERK1/2, p-ERK1/2 and TGF-β receptor I. Immunohistochemistry was used to examine the expression of CTGF. Compared with the model group, increasing concentrations of Corilagin improved the quality of life, inhibited the mRNA expression of miR-21, promoted smad7 protein expression, and inhibited CTGF protein expression (p < 0.05 or 0.01). Moreover, Corilagin significantly reduced the protein levels of p-smad1, p-smad2, p-ERK1/2, and TGF-β receptor I (p < 0.05 or 0.01). CTGF staining in the cytoplasm was markedly decreased by Corilagin (p < 0.05 or 0.01). In conclusion, Corilagin inhibited schistosomiasis-induced hepatic fibrosis via the miR21/smad7/ERK pathway in this animal model. |
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