Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway
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 isoflavo...
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| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Behavioural Neurology |
| Online Access: | http://dx.doi.org/10.1155/2018/1960106 |
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| author | Ling-yun Wu Zhen-nan Ye Zong Zhuang Yongyue Gao Chao Tang Chen-hui Zhou Chun-xi Wang Xiang-sheng Zhang Guang-bin Xie Jing-peng Liu Meng-liang Zhou Chun-hua Hang Ji-xin Shi |
| author_facet | Ling-yun Wu Zhen-nan Ye Zong Zhuang Yongyue Gao Chao Tang Chen-hui Zhou Chun-xi Wang Xiang-sheng Zhang Guang-bin Xie Jing-peng Liu Meng-liang Zhou Chun-hua Hang Ji-xin Shi |
| author_sort | Ling-yun Wu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-d3f080c031984d37aa4a1d39d806e3ea |
| institution | Kabale University |
| issn | 0953-4180 1875-8584 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Behavioural Neurology |
| spelling | doaj-art-d3f080c031984d37aa4a1d39d806e3ea2025-02-03T01:30:30ZengWileyBehavioural Neurology0953-41801875-85842018-01-01201810.1155/2018/19601061960106Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB PathwayLing-yun Wu0Zhen-nan Ye1Zong Zhuang2Yongyue Gao3Chao Tang4Chen-hui Zhou5Chun-xi Wang6Xiang-sheng Zhang7Guang-bin Xie8Jing-peng Liu9Meng-liang Zhou10Chun-hua Hang11Ji-xin Shi12Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province 510260, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Southern Medical University (Guangzhou), Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East ZhongShan Road, Nanjing, Jiangsu Province 210002, ChinaInflammatory 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.http://dx.doi.org/10.1155/2018/1960106 |
| spellingShingle | Ling-yun Wu Zhen-nan Ye Zong Zhuang Yongyue Gao Chao Tang Chen-hui Zhou Chun-xi Wang Xiang-sheng Zhang Guang-bin Xie Jing-peng Liu Meng-liang Zhou Chun-hua Hang Ji-xin Shi Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway Behavioural Neurology |
| title | Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway |
| title_full | Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway |
| title_fullStr | Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway |
| title_full_unstemmed | Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway |
| title_short | Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway |
| title_sort | biochanin a reduces inflammatory injury and neuronal apoptosis following subarachnoid hemorrhage via suppression of the tlrs tirap myd88 nf κb pathway |
| url | http://dx.doi.org/10.1155/2018/1960106 |
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