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Med Sci Monit. 2019 Nov 26;25:8975-8983. doi: 10.12659/MSM.918665.

Biochanin A Provides Neuroprotection Against Cerebral Ischemia/Reperfusion Injury by Nrf2-Mediated Inhibition of Oxidative Stress and Inflammation Signaling Pathway in Rats.

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Key Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin, Guangxi, China (mainland).
Department of Pathology and Physiopathology, Guilin Medical University, Guilin, Guangxi, China (mainland).
Department of Radiation Oncology of Clinical Cancer Center, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China (mainland).
Department of Neurosurgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China (mainland).
Department of Physiology, Guilin Medical University, Guilin, Guangxi, China (mainland).
Functional Laboratory, Guilin Medical University, Guilin, Guangxi, China (mainland).


BACKGROUND Oxidative stress and neuroinflammation are 2 pivotal mechanisms in the progression of cerebral ischemia/reperfusion injury. Biochanin A, a natural phytoestrogen, has been reported to protect against ischemic brain injury in animal experiments, but the possible pharmacological mechanisms of its neuroprotection remain elusive. In this research, we sought to investigate the neuroprotective effects of biochanin A in experimental stroke rats and the probable mechanisms underlying oxidative stress and inflammation signaling pathways. MATERIAL AND METHODS An ischemic stroke model was induced by inserting thread into the middle cerebral artery. Rats were pre-administered intraperitoneally with a vehicle solution or biochanin A (10, 20, or 40 mg·kg·d--⁻¹) for 14 days prior to ischemic stroke. Neurological score, infarct volume, and cerebral edema were assessed after 2 h of ischemia and 24 h of reperfusion. The activities of SOD and GSH-Px and MDA content were measured. The expressions of Nrf2, HO-1, and NF-kappaB and the activity of phosphor-IkappaBalpha were detected by Western blotting. RESULTS Biochanin A pretreatment significantly improved neurological deficit and decreased infarct size and brain edema. Biochanin A also enhanced SOD and GSH-Px activities and suppressed the production of MDA. Additionally, biochanin A promoted Nrf2 nuclear translocation, promoted the expression of HO-1, and inhibited NF-kappaB activation in ischemic brain injury. CONCLUSIONS The results indicated that biochanin A protected the brain against ischemic injury in rats by anti-oxidative and anti-inflammatory actions. The activation of the Nrf2 pathway and the inhibition of the NF-kappaB pathway may contribute to the neuroprotective effects of biochanin A.

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