D-Carvone inhibit cerebral ischemia/reperfusion induced inflammatory response TLR4/NLRP3 signaling pathway.

Abstract To explore the present treatment strategies for ischemic stroke lowered by ischemia-reperfusion (I/R) injury, to hypothesize the effect of d -Carvone on cerebral I/R brain injury induced neuroinflammation through oxidative stress markers mechanism via NRLP3 and TLR4 marker expressions in rat model. The rats were divided into four groups: Sham, I/R vehicle, I/R + D-carvone (10 mg/kg/bw), I/R + D-carvone (20 mg/kg/bw). Supplementation of d -carvone at dose of 10 and 20 m/kg/bw increased the water content, reduced infract volume, attenuated neurological score depicts, furthermore it had antioxidative, anti-inflammatory, and anti-apoptotic effects against cerebral I/R brain injury. In the brain tissues decreased proinflammatory cytokines IL-1β and TNF-α reduced interleukins IL-6, IL-4, IL-10 & VEGF dose dependently, and mRNA expressions of NLRP3, caspase -1, TNF-α, ASC, IL-1β and TLR3 down regulated in cerebral I/R induced rats. Finally d - carvone can successfully improve the cerebral I/R induced rats neuroinflammation, in the hippocampus and cortical areas of the brain finally reduces cerebral I/R induced injury. These results were hypothesized that d -carvone contributed to cerebral stroke associated with the TLR3, giving an excellent therapeutic approach for cerebral I/R brain injury.