Excessive neuroinflammation mediated by microglia has a detrimental effect on the progression of ischemic stroke. Eriocalyxin B (EriB) was found with a neuroprotective effect in mice with Parkinson’s disease by suppressing the microglial overactivation. This study aims to investigate the roles of EriB in permanent middle cerebral artery occlusion (pMCAO) mice. The pMCAO was induced by intraluminal filament method in internal carotidartery of mice, which underwent an immediately intraperitoneal injection of EriB (10 mg/kg) post surgery. The behavior score, 2,3,5-triphenyltetrazole chloride staining, Nissl staining, TUNEL, immunohistochemistry, immunofluorescence, PCR, ELISA and immunoblotting revealed that EriB administration reduced brain infarct and neuron death, ameliorated neuroinflammation and microglia overactivation in pMCAO mice, manifested by alterations of TUNEL-positive cell numbers, ionized calcium binding adaptor molecule 1 (Iba-1)-positive cell numbers, expression of tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase and arginase 1. In addition, EriB suppressed ischemia-induced activation of nuclear factor kappa B (NF-κB) signaling in brain penumbra, suggesting the involvement of NF-κB in EriB function. In conclusions, EriB exerted anti-inflammatory effects in ischemia stroke through regulating NF-κB signaling pathway, which may provide insights into the neuroprotective effect of EriB on the treatment of ischemic stroke.
