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作 者:Hanaa F.B.Gaber Mohamed K.Mahfouz Fatma SM Moawed Esraa SA Ahmed Omayma AR Abo-Zaid
机构地区:[1]Biochemistry and Molecular Biology Department,Faculty of Vet Medicine Benha University,Banha,Egypt [2]Health Radiation Research,National Center for Radiation Research and Technology,Egyptian Atomic Energy Authority,Cairo,Egypt [3]Radiation Biology Research,National Center for Radiation Research and Technology,Atomic Energy Authority,Cairo,Egypt
出 处:《Asian Pacific Journal of Tropical Biomedicine》2025年第4期150-157,共8页亚太热带生物医学杂志(英文版)
摘 要:Objective:To investigate the effects of quercetin on inflammatory signaling pathways and hepatic oxidative injury using a streptozotocin-induced liver injury model.Methods:Four groups of 32 rats were used in this study:three groups were given streptozotocin to induce diabetes,and one group was given a normal control.For treatment groups,each group received either metformin(200 mg/kg body weight)or quercetin(50 mg/kg body weight)for a month.The expression of SREBP1c was detected by quantitative RT-PCR and fibrosis-related proteins(TGF-βand p-Smad3)was evaluated by Western blot.Furthermore,MCP and IL-1βwere determined by ELISA.Results:Quercetin significantly reduced insulin and glucose levels.Besides,it reduced the serum levels of ALT,AST,and ALP,improved lipid profile,lowered the MDA level,increased SOD activity,decreased the rise in MCP-1 and IL-1β,inhibited the TGF-β/Smad3 signaling pathway,decreasedα-SMA and SREBP1c expression,and increased AMPK(P<0.05).Conclusions:Quercetin could significantly mitigate hepatic damage by modulating the expression of pro-inflammatory cytokines and fibrosis markers.
关 键 词:QUERCETIN METFORMIN STREPTOZOTOCIN Liver injury TGF-β/Smad signaling AMPK SREBP1c
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