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Ischemic stroke is one of the leading causes of mortality and disability worldwide. However, there is a current lack of effective therapies available. As the resident macrophages of the brain, microglia can monitor the microenvironment and initiate immune responses. In response to various brain injuries, such as ischemic stroke, microglia are activated and polarized into the proinflammatory M1 phenotype or the anti‑inflammatory M2 phenotype. The immunomodulatory molecules, such as cytokines and chemokines, generated by these microglia are closely associated with secondary brain damage or repair, respectively, following ischemic stroke. It has been shown that M1 microglia promote secondary brain damage, whilst M2 microglia facilitate recovery following stroke. In addition, autophagy is also reportedly involved in the pathology of ischemic stroke through regulating the activation and function of microglia. Therefore, this review aimed to provide a comprehensive overview of microglia activation, their functions and changes, and the modulators of these processes, including transcription factors, membrane receptors, ion channel proteins and genes, in ischemic stroke. The effects of autophagy on microglia polarization in ischemic stroke were also reviewed. Finally, future research areas of ischemic stroke and the implications of the current knowledge for the development of novel therapeutics for ischemic stroke were identified.

Coagulation factor XII (FXII) is a multidomain serine protease that is the starter of intrinsic coagulation pathway. FXII deficiency and clinical hemostasis are not associated with bleeding, so investigators have not considered FXII important in physiology for a long time. In seeking explanation for FXII-independent physiologic hemostasis, investigators found FXII is an essential constitute of contact system that mediates procoagulation and proinflammatory via the intrinsic coagulation pathway or the Kallikrein-kinin system, respectively. Date obtained in infectious inflammation have revealed FXII mediated clotting that limited bacterial or toxin spread in early phases, and regulated fibrinolysis in later. Moreover, FXII mediated two non- infectious inflammation Hereditary angioedema (HAE) and non-specific allergy via bradykinin (BK) formation. In the coagulation, thrombosis not only is involved with coagulation, but is redefined as thrombo-inflammatory disorder. This paper reviews in det ail the progresses in roles of FXII intersection between inflammation and coagulation.

The expression of Ferroportin (Fpn) was examined at different time points in rats following focal cerebral ischemia treated with or without the traditional Chinese medicine Naotaifang. Initially, rats were randomly divided into 2, 6, 12, 24 and 72 h groups following middle cerebral artery occlusion (MCAO) and the mRNA and protein level of Fpn was detected by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) at the above time points. Secondly, the rats were randomly divided into five groups as follows: Sham surgery group, model group, low-dose group (3 g/kg NTE), medium dose group (9 g/kg NTE) and the high-dose group (27 g/kg NTE). After 3 days of corresponding therapy by intragastric administration once a day, the regional cerebral ischemia model was reproduced by the MCAO suture method. On the third day, the neurological behavior of the rats was analyzed by neurobehavioral assessment. Fpn in the hippocampal CA2 region was measured by immunohistochemistry and the mRNA level of Fpn was detected by RT-PCR. Expression of Fpn in the hippocampal CA2 region reached a peak 12 h after surgery (P