Codonopis bulleynana Forest ex Diels (cbFeD) effectively attenuates hepatic fibrosis in CCl4-induced fibrotic mice model

Biomedicine & Pharmacotherapy

卷:133

Dechang Mao¹  Yue Xing²  Huaning Wang³  Yunpeng Luan⁴  Xiang Li⁴  Yunqi Luan⁵  Lu Ying⁵  Shuangqing Zheng⁵  Chunyan Li⁵  Yanmei Li⁵  Zhipeng Li⁵  Hongmin Wang⁶  Junbo Hu⁷  Zhuoya Li⁷  Mei Xu⁸ 

[1] Department of Gastrointestinal Surgery Center and Department of Laboratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;

[2] Department of Pi-wei Disease, The First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming 650021, China;

[3] Department of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

[4] Department of Life Technology Teaching and Research, School of Life Science, Southwest Forestry University, Kunming 650224, China;

[5] Faculty of Soil Science, Department of Geography and Ecology Lomonosov Moscow State University, Russia;

[6] KPC Pharmaceuticals, Inc, Kunming 650106, China;

[7] Yunnan Yisheng Pharmaceutical Co., Ltd., Kunming 650000, China;

关键词: Codonopis bulleynana Forest ex Diels;    Liver injury;    Fibrogenesis;    Inflammation;    Hepatic stellate cell;   

DOI  :  

来源: DOAJ

【 摘 要 】

The root of Codonopis bulleynana Forest ex Diels (cbFeD), a tonic food widely used in Yunnan Province of China, was found to have a wide range of pharmacological effects. The present study was designed to investigate the anti-fibrotic effect of water extracts of cbFeD in chronic liver injury mice model induced by carbon tetrachloride (CCl4) and to explore its underlying mechanisms. Phytochemical analysis revealed multiple components were present in the water extract of cbFeD and the compounds were mostly enriched in organic acid and its derivatives, flavone, amino acid derivatives, nucleotide and its derivatives, carbohydrates etc. Treatment with cbFeD significantly attenuated liver injury and fibrosis in CCl4-administered mice evidenced by improved liver histology, ameliorated apoptosis of hepatocytes, and decreased transaminase levels in the serum. Decreased activities of superoxide dismutase (SOD) and catalase (CAT) were markedly reversed upon treatment with cbFeD while levels of malondialdehyde (MDA) and glutathione (GSH) were significantly restored towards normal values. cbFeD also suppressed intrahepatic inflammatory cell infiltration and Kupffer cell activation. Furthermore, our study revealed an inhibitory effect of cbFeD on hepatic stellate cells (HSCs) activation both in vitro and in vivo. In conclusion, cbFeD could exert a protective role against liver fibrosis in mice model induced by CCl4 that is comparable to the positive control silymarin and might be developed into a promising anti-fibrotic drug.

【 授权许可】

Unknown