Research progress on the modulation mechanism of electroacupuncture for learning and memory impairment after ischemic stroke / 中国针灸

Electroacupuncture may play a role in treatment of learning and memory impairment after ischemic stroke by regulating phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA)/cAMP response element binding protein (CREB) signaling pathway, nerve growth factor (NGF)/tyrosine kinase-A (TrkA) signaling pathway, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, Notch signaling pathway, erythropoietin-producing hepatocyte (Eph)/ephrin signaling pathway. The interactions among these pathways should be further explored in treatment of learning and memory impairment after ischemic stroke.

Role of angiotensin Ⅱ-angiotensin Ⅱ receptor 1 pathway on inflammatory activation in the lung of rats / 中华急诊医学杂志

Objective To investigate the potential role of angiotensinⅡ(AngⅡ)-angiotensinⅡreceptor 1 (ATRI) pathway on inflammatory activation in the lung of rats. Method Twenty four Sprague-Dawley rats were randomly divided into four groups: control group, Ang II group, AngⅡ+losartan group and losartan group. Lung wet/dry weight (W/D) was recorded to assess lung injury. The total lung homogenates were prepared to detect nuclear factor-kappa B (NF-?B) activation by electrophoretic mobility gel shift assary (EMSA), tumor necrosis factor (TNF)-?mRNA expression by reverse transcription polymerase chain reaction (RT-PCR), myeloperoxidase (MPO) and malondialdehyde (MDA) by colorimetry. Plasma yon Willebrand Factor (vWF) were assessed by enzyme-linked immunosorbent assay (ELISA). Meanwhile, pathological changes were examined under optical microscope. Results Histologically, alveolar edema, hemorrhage, and massive inflammatory cell infiltration were observed in AngⅡgroup, but not in control group and losartan group. Compared with AngⅡgroup, histological injury was lesser in AngⅡ+ losartan group. In AngⅡgroup, lung W/D, NF-?B activation, TNF-?mRNA expression, MPO, MDA and vWF were markedly higher than those in the other three groups. There were not significant differences of lung W/D, NF-?B activation, TNF-?mRNA expression, MPO, MDA and vWF in control group, AngⅡ+ losartan group and losartan group. Conclusions Systemic infusion of AngⅡcould up- regulate inflammatory mediator expression and induce lung injury in rats. AngⅡ, acting mainly through ATRI, induced inflammatory activation in the lung of rats.