Author/Authors :
Wu, Ling-yun Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Ye, Zhen-nan Department of Neurosurgery - the Second Affiliated Hospital of Guangzhou Medical University - Guangdong Province, China , Zhuang, Zong Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Gao, Yongyue Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Tang, Chao Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Zhou, Chen-hui Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Wang, Chun-xi Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Zhang, Xiang-sheng Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Liu, Jing-peng Department of Neurosurgery - Jinling Hospital - School of Medicine - Southern Medical University (Guangzhou), Jiangsu Province, China , Zhou, Meng-liang Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Hang, Chun-hua Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China , Shi, Ji-xin Department of Neurosurgery - Jinling Hospital - School of Medicine - Nanjing University, Jiangsu Province, China
Abstract :
Inflammatory injury and neuronal apoptosis participate in the period of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Suppression of inflammation has recently been shown to reduce neuronal death and neurobehavioral dysfunction post SAH. Biochanin A (BCA), a natural bioactive isoflavonoid, has been confirmed to emerge the anti-inflammatory pharmacological function. This original study was aimed at evaluating and identifying the neuroprotective role of BCA and the underlying molecular mechanism in an experimental Sprague-Dawley rat SAH model. Neurobehavioral function was evaluated via the modified water maze test and modified Garcia neurologic score system. Thus, we confirmed that BCA markedly decreased the activated level of TLRs/TIRAP/MyD88/NF-κB pathway and the production of cytokines. BCA also significantly ameliorated neuronal apoptosis which correlated with the improvement of neurobehavioral dysfunction post SAH. These results indicated that BCA may provide neuroprotection against EBI through the inhibition of inflammatory injury and neuronal apoptosis partially via the TLRs/TIRAP/MyD88/NF-κB signal pathway.
