Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism[J]
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- Niu Chengwei
- hanghai Key Laboratory of Complex Prescription, The MOE Key Laboratory for Standardization of Chinese Medicines, and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine
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- Sheng Yuchen
- Center for Drug Safety Evaluation and Research, Shanghai University of Traditional Chinese Medicine
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- Zhu Enyuan
- hanghai Key Laboratory of Complex Prescription, The MOE Key Laboratory for Standardization of Chinese Medicines, and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine
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- Ji Lili
- hanghai Key Laboratory of Complex Prescription, The MOE Key Laboratory for Standardization of Chinese Medicines, and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine
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- Wang Zhengtao
- hanghai Key Laboratory of Complex Prescription, The MOE Key Laboratory for Standardization of Chinese Medicines, and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine
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- タイトル別名
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- Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism
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<p>The rhizome of Dioscorea bulbifera Linn, traditionally used to treat thyroid disease and cancer in China, is reported to induce serious liver injury during clinical practice. Diosbulbin B (DB), a diterpene lactone, has been found to be the main toxic compound in D. bulbifera. The present study aims to investigate the protection of ferulic acid (FA) against DB-induced acute liver injury and its engaged mechanism. Mice were orally administered FA (20, 40, 80 mg/kg) once daily for 6 consecutive days; and then orally given DB (250 mg/kg) on the last day. Daily FA (40, 80 mg/kg) decreased DB (250 mg/kg)-induced increase in serum levels of alanine/aspartate aminotransferase (ALT/AST) and alkaline phosphatase (ALP). Histological evaluation showed that FA (80 mg/kg) ameliorated DB-induced hepatocellular degeneration and lymphocyte infiltration. Results of terminal dUTP nick-end labeling (TUNEL) staining assay showed that FA (80 mg/kg) decreased the DB-increased number of apoptotic hepatocytes. FA (40, 80 mg/kg) reduced DB-increased liver malondialdehyde (MDA) amount. FA (40, 80 mg/kg) decreased DB-increased serum levels of tumor necrosis factor alpha (TNF-α) and interferon-γ (IFN-γ), and liver myeloperoxidase (MPO) activity. FA (80 mg/kg) reversed the DB-induced decrease in expression of inhibitor of kappa B (IκB) and the increase in nuclear translocation of the p65 subunit of nuclear factor kappa B (NFκBp65). Taken together, our results demonstrate that FA prevents DB-induced acute liver injury via inhibiting intrahepatic inflammation and liver apoptosis.</p>
収録刊行物
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- BioScience Trends
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BioScience Trends 10 (5), 386-391, 2016
特定非営利活動法人 バイオ＆ソーシャル・サイエンス推進国際研究交流会