Regulation Microglia Activation Mediated Neuroinflammation to Ameliorate Ischemia-reperfusion Injury via STAT5-NF-kappa B Pathway in Ischemic Stroke

Authors
Z Pu, S Xia, P Shao et al

Lab
Nanjing University, Nanjing, P.R. China

Journal
Brain Sciences

Abstract
Inflammatory reaction after ischemia-reperfusion contributes significantly to prognosis, and microglia activation is the main resource of inflammation in nervous system. STAT5 is proving to be a highly effective anti-inflammatory therapy with great potential, and inhibition of STAT5 has demonstrated significant anti-inflammation and therapeutic effects, but rarely focus on mechanism of neuroinflammation and brain injury from ischemia-reperfusion. It is the first time to found that the anti-inflammation of dauricine is mainly through STAT5-NF-kappa B pathway, might act as a STAT5 inhibitor. Dauricine suppressed the inflammation cytokines Eotaxin, KC, TNF-alpha, IL-1alpha, IL-1beta, IL-6, IL-12beta, IL-17alpha, and also inhibited the microglia activation. STAT5b mutant at Tyr-699 reversed the protective effect of dauricine on oxygen-glucose deprivation-reperfusion injury of neurons, and re activated the suppression of dauricine on P-NF-kappa B of microglia. These results suggest that dauricine might suppress the neuroinflammation and protect the neuron from the injury of post-ischemia reperfusion via mediating the microglia activation through STAT5-NF-kapp B pathway, and as a potential therapeutic target for neuroinflammation, STAT5 needs to be raised concern in ischemic stroke

BIOSEB Instruments Used:
Grip strength test (BIO-GS3)