引用大鼠ELISA科研检测试剂盒的文献

IF：7.675

Abstract:Cerebral ischemia/reperfusion causes exacerbated neuronal damage involving excessive neuroinflammation and oxidative stress. ROS is considered a signal molecule to activateNLRP3; thus, the ROS/NLRP3/pyroptosis axis plays a vital role in the pathogenesis of cerebral ischemia/reperfusion injury (CIRI). Therefore, targeting the inhibition of the ROS/NLRP3/pyroptosisaxis may be a promising therapeutic tactic for CIRI.Epimedium(EP) contains many active ingredients(ICA, ICS II, and ICT), which have a wide range of pharmacological activities. However, whetherEP can protect against CIRI remains unknown. Thus, in this study, we designed to investigatethe effect and possible underlying mechanism of EP on CIRI. The results showed that treatmentwith EP dramatically mitigated brain damage in rats following CIRI, which was achieved by suppressing mitochondrial oxidative stress and neuroinflammation. Furthermore, we identified theROS/NLRP3/pyroptosis axis as a vital process and NLRP3 as a vital target in EP-mediated protection.Most interestingly, the main compounds of EP directly bonded with NLRP3, as reflected by molecular docking, which indicated that NLRP3 might be a promising therapeutic target for EP-elicitedcerebral protection. In conclusion, our findings illustrate that ICS II protects against neuron loss andneuroinflammation after CIRI by inhibiting ROS/NLRP3-mediated pyroptosis.