Objective: To investigate the effect of genistein on the proliferation and lipid peroxidation of hepatic stellate cells (HSC) in vitro and its the protective effect against hepatic fibrosis.
Methods: Rat hepatic stellate cells (HSC-T6 cells) were divided into 3 groups and incubated in the presence of 0.1 mol/L hydrogen dioxide followed by washing with PBS for 3 times. Genistein at different concentrations was added into the cell culture meclia, and after 48 h of incubation, the cell proliferation was assessed with MTT assay and the levels of superoxide dismutase (SOD), malonaldehyde (MDA), glutathione (GSH) and glutathione peroxidase (GSH-PX) in the supernatant of the cell culture were measured.
Results: Genistein at different concentrations inhibited the cell proliferation, showing a dose-effect relationship. Genistein significantly decreased the production of intracellular MDA and GSH and increased SOD and GSH PX activity.
Conclusion: Genistein can prevent the formation of hepatic fibrosis probably by decreasing HSC proliferation and lipid peroxidation.
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Cell Metab
January 2025
Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, 410008 Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, 410008 Changsha, Hunan, China; FuRong Laboratory, 410078 Changsha, Hunan, China. Electronic address:
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Department of Anesthesiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
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Departamento de Innovación Biomédica, Centro de Investigación Científica y de Educación Superior de Ensenada, Baja California (CICESE), Carretera Ensenada-Tijuana No. 3918, Zona Playitas, C.P. 22860, Ensenada, Baja California, Mexico.
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Department of Radiation Oncology, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, China.
Ginsenoside Rd (Rd) is a bioactive compound predominantly found in Panax ginseng C.A. Meyer and Panax notoginseng (Burkill) F.
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Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China. Electronic address:
Hepatic stellate cells (HSCs) are the central link of the occurrence and development of hepatic fibrosis, and autophagy promotes HSCs activation. N6-methyladenosine (m6A) RNA modification can also control autophagy by targeting selected autophagy-associated genes. but up to now, little research has been done on the m6A modification autophagy-related genes (ATGs) in hepatic fibrosis.
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