Journal of ethnopharmacology · 2022
Sanhuang xiexin decoction ameliorates secondary liver injury in DSS-induced colitis involve regulating inflammation and bile acid metabolism.
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Li Lixia, Wang Yingjie, Zhao Ling, Ye Gang, Shi Fei, Li Yinglun, Zou Yuanfeng, Song Xu, Zhao Xinghong, Yin Zhongqiong, Wu Xueyuan, Li Wen, Tang Huaqiao
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: SanHuang XieXin decoction (SXD) is a widely applicated traditional Chinese medicine (TCM) with a significant gut-liver axis regulation effect.
AIM OF THE STUDY: To evaluate the therapeutic effect and elucidate the possible underlying molecular mechanisms of SXD on liver damage secondary to ulcerative colitis (UC) in mice.
MATERIALS AND METHODS: A model of liver damage secondary to UC was induced by drinking 5% dextran sodium sulfate (DSS) in mice. These mice were treated with one of three doses of SXD or sulfasalazine (SASP), then liver samples were collected and tested.
RESULTS: The results reveal that SXD treatment reduced liver cells swelling, and inhibited the accumulation of the hepatic-pro-inflammatory cytokines IL-1β and tumor necrosis factor-α (TNF-α) in mice with colitis. In addition, SXD reduced the production of nitric oxide (NO) and malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD). In inflammation regulating, SXD significantly down regulated the protein expression of MyD88 and p-Iκα, but upregulated Iκα. In bile acid metabolism regulating, SXD significantly down regulated the protein expression of FXR, MRP2, BESP and SHP. Therefore, SXD treatment can regulate the TLR4-NF-κB and bile acid metabolism pathways to alleviate liver inflammation and cholestasis.
CONCLUSIONS: These results demonstrate that SXD is a potential alternative therapeutic medicine for the treatment of liver damage secondary to colitis.
AIM OF THE STUDY: To evaluate the therapeutic effect and elucidate the possible underlying molecular mechanisms of SXD on liver damage secondary to ulcerative colitis (UC) in mice.
MATERIALS AND METHODS: A model of liver damage secondary to UC was induced by drinking 5% dextran sodium sulfate (DSS) in mice. These mice were treated with one of three doses of SXD or sulfasalazine (SASP), then liver samples were collected and tested.
RESULTS: The results reveal that SXD treatment reduced liver cells swelling, and inhibited the accumulation of the hepatic-pro-inflammatory cytokines IL-1β and tumor necrosis factor-α (TNF-α) in mice with colitis. In addition, SXD reduced the production of nitric oxide (NO) and malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD). In inflammation regulating, SXD significantly down regulated the protein expression of MyD88 and p-Iκα, but upregulated Iκα. In bile acid metabolism regulating, SXD significantly down regulated the protein expression of FXR, MRP2, BESP and SHP. Therefore, SXD treatment can regulate the TLR4-NF-κB and bile acid metabolism pathways to alleviate liver inflammation and cholestasis.
CONCLUSIONS: These results demonstrate that SXD is a potential alternative therapeutic medicine for the treatment of liver damage secondary to colitis.