Biochanin A protects against focal cerebral ischemia/reperfusion in rats via inhibition of p38-mediated inflammatory responses

•Biochanin A has been shown to have neuroprotective effects in cerebral ischemia/reperfusion rats.•Biochanin A decreases the release of pro-inflammatory mediators in ischemia/reperfusion.•The neuroprotective effects of biochanin A may be related to its inhibiting p38-mediated inflammatory responses.•Biochanin A may have potential as a therapeutic agent for cerebral ischemia/reperfusion injury.

Biochanin A, an O-methylated natural isoflavonoid classified as phytoestrogen, has been reported to show anti-tumorigenesis, anti-oxidation, and anti-inflammatory properties. However, little is known about the effects of biochanin A on cerebral ischemia/reperfusion. In this study, the neuroprotective and anti-inflammatory effects of biochanin A against ischemia/reperfusion injury, as well as the related molecular mechanisms, were investigated in rat models. Male Sprague–Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h, followed by 24 h of reperfusion. Then neurological deficits, infarct volume and brain edema were evaluated. The MPO activity and TNF-α and IL-1β levels in ischemic boundary zone were determined by a spectrophotometer and the enzyme-linked immunosorbent assay (ELISA). The expressions of TNF-α, IL-1β, and phosphorylation of p38 were measured by RT-PCR or Western blotting. Consequently, our findings showed that biochanin A treatment for 14 days had significantly reduced infarct volume and brain edema, and improved neurological deficits in focal cerebral ischemia/reperfusion rats. The MPO activity and TNF-α and IL-1β levels were greatly increased after ischemia/reperfusion injury, while treatment with biochanin A dramatically suppressed these inflammatory processes. Furthermore, biochanin A attenuated the increase in p-p38 level in the ischemia/reperfusion brain tissue. Taken together, biochanin A has been shown to have neuroprotective effects in cerebral ischemia/reperfusion, and the mechanisms may correlate with inhibiting inflammatory response, as well as the inactivation of p38 signaling pathway.