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作 者:Xigong Li Jing Fu Ming Guan Haifei Shi Wenming Pan Xianfeng Lou
机构地区:[1]Department of Orthopedics,The First Affiliated Hospital of Zhejiang University,Hangzhou,Zhejiang Province,China [2]Department of Stomatology,Xixi Hospital,Hangzhou,Zhejiang Province,China [3]Department of Orthopedics,and Spine Surgery,the Affiliated Hospital of Xuzhou Medical School,the Second People’s Hospital of Changshu,Changshu,Jiangsu Province,China
出 处:《Neural Regeneration Research》2024年第9期2050-2056,共7页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundation of China,Nos.LY20H090018(to XL)and LY20H060008(to HS).
摘 要:Previous studies have shown that Biochanin A,a flavonoid compound with estrogenic effects,can serve as a neuroprotective agent in the context of cerebral ischemia/reperfusion injury;howeve r,its effect on spinal cord injury is still unclea r. In this study,a rat model of spinal cord injury was established using the heavy o bject impact method,and the rats were then treated with Biochanin A(40 mg/kg) via intrape ritoneal injection for 14 consecutive days.The res ults showed that Biochanin A effectively alleviated spinal cord neuronal injury and spinal co rd tissue injury,reduced inflammation and oxidative stress in spinal cord neuro ns,and reduced apoptosis and pyroptosis.In addition,Biochanin A inhibited the expression of inflammasome-related proteins(ASC,NLRP3,and GSDMD)and the Toll-like receptor 4/nuclear factor-κB pathway,activated the Nrf2/heme oxygenase 1 signaling pathway,and increased the expression of the autophagy markers LC3 Ⅱ,Beclin-1,and P62.Moreove r,the therapeutic effects of Biochanin A on early post-s pinal cord injury were similar to those of methylprednisolone.These findings suggest that Biochanin A protected neurons in the injured spinal cord through the Toll-like receptor 4/nuclear factor κB and Nrf2/heme oxygenase 1 signaling pathways.These findings suggest that Biochanin A can alleviate post-spinal cord injury at an early stage.
关 键 词:apoptosis AUTOPHAGY Biochanin A heme oxygenase 1 INFLAMMATION Nrf2 protein nuclear factor kappa-B oxidative stress spinal cord injury Toll-like receptor 4
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