Aim: Ginkgolide B (GB) has shown ne

Aim: Ginkgolide B (GB) has shown neuroprotective effect in treating ischemic stroke,related to its property of anti-inflammation. Nevertheless, it is unclear whether GB is able tomodulate microglia/macrophage polarization, which has recently been proven to be vital inthe pathology of ischemic stroke. Methods: We performed transient middle cerebral arteryocclusion (tMCAO) on C57BL/6J male mice and induced cultured BV2 microglia and primarybone marrow-derived macrophages to be M1/2 phenotype by LPS+ interferon-c andIL-4, respectively. Immunofluorescence and flow cytometry were used for detecting thespecialized protein expression of M1/2, such as CD206 and CD16/32. qPCR was utilized todetect the signature gene change of M1/2. Results: GB significantly reduced cerebralischemic damage and ameliorated the neurological deficits of mice after tMCAO. Moreimportantly, our experiments proved that GB promoted microglia/macrophage transferringfrom inflammatory M1 phenotype to a protective, anti-inflammatory M2 phenotype in vivoor vitro. CV3988 and silencing the platelet activator factor (PAF) receptor by siRNA demonstratedthat PAF receptor was involved in the modulation of microglia/macrophage polarization.Conclusion: Our results reveal a novel pharmacological effect of GB in modulatingmicroglia/macrophage polarization after tMCAO, thus deepening our understanding ofneuroprotective mechanisms of GB in treatment of ischemic stroke. Furthermore, this newmechanism may allow GB to be used in many other microglia/macrophage polarizationrelatedinflammatory diseases.

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结果 (简体中文) 1: [复制]

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目的：银杏内酯B（GB）在治疗缺血性中风方面显示出神经保护作用， 与其抗炎特性有关。然而，目前尚不清楚GB是否能够 调节小胶质细胞/巨噬细胞的极化，近来已被证明在 缺血性中风的病理学中至关重要。方法：我们 对C57BL / 6J雄性小鼠进行了短暂的大脑中动脉闭塞（tMCAO），并 通过LPS +干扰素-c和 IL-4分别诱导培养的BV2小胶质细胞和原代骨髓来源的巨噬细胞为M1 / 2表型。免疫荧光和流式细胞仪用于检测 M1 / 2 的特定蛋白表达，例如CD206和CD16 / 32。qPCR用于 检测M1 / 2的特征基因变化。结果：GB显着降低 了tMCAO后小鼠的脑缺血损伤并减轻了其神经功能缺损。更 重要的是，我们的实验证明，GB可以 在体内 或体外促进小胶质细胞/巨噬细胞从炎症M1型转变为保护性抗炎症M2型。CV3988和通过siRNA沉默血小板激活因子（PAF）受体证明 PAF受体参与小胶质细胞/巨噬细胞极化的调节。 结论：我们的结果揭示了GB在 tMCAO后调节小胶质细胞/巨噬细胞极化方面的新药理作用，从而加深了我们对 GB治疗缺血性中风的神经保护机制。此外，这种新 机制可能使GB可以用于许多其他小胶质细胞/巨噬细胞极化相关的 炎症性疾病。

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结果 (简体中文) 2:[复制]

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Aim: Ginkgolide B (GB) has shown neuroprotective effect in treating ischemic stroke, related to its property of anti-inflammation. Nevertheless, it is unclear whether GB is able to modulate microglia/macrophage polarization, which has recently been proven to be vital in the pathology of ischemic stroke. Methods: We performed transient middle cerebral artery occlusion (tMCAO) on C57BL/6J male mice and induced cultured BV2 microglia and primary bone marrow-derived macrophages to be M1/2 phenotype by LPS+ interferon-c and IL-4, respectively. Immunofluorescence and flow cytometry were used for detecting the specialized protein expression of M1/2, such as CD206 and CD16/32. qPCR was utilized to detect the signature gene change of M1/2. Results: GB significantly reduced cerebral ischemic damage and ameliorated the neurological deficits of mice after tMCAO. More importantly, our experiments proved that GB promoted microglia/macrophage transferring from inflammatory M1 phenotype to a protective, anti-inflammatory M2 phenotype in vivo or vitro. CV3988 and silencing the platelet activator factor (PAF) receptor by siRNA demonstrated that PAF receptor was involved in the modulation of microglia/macrophage polarization. Conclusion: Our results reveal a novel pharmacological effect of GB in modulating microglia/macrophage polarization after tMCAO, thus deepening our understanding of neuroprotective mechanisms of GB in treatment of ischemic stroke. Furthermore, this new mechanism may allow GB to be used in many other microglia/macrophage polarizationrelated inflammatory diseases.

正在翻译中..

结果 (简体中文) 3:[复制]

复制成功！

目的：银杏内酯B（GB）对缺血性脑卒中具有神经保护作用， 与其抗炎作用有关。然而，目前尚不清楚国标是否能够 调节小胶质细胞/巨噬细胞极化，最近被证明在 缺血性中风的病理学。方法：采用短暂性大脑中动脉 用C57BL/6J雄性小鼠阻断（tMCAO）诱导BV2小胶质细胞和原代培养 骨髓源性巨噬细胞经LPS+ifn-c鉴定为M1/2表型 分别是IL-4。免疫荧光法和流式细胞术检测各组大鼠的血清白蛋白水平 M1/2的特异性蛋白表达，如CD206和CD16/32。qPCR用于 检测M1/2的标志性基因改变。结果：GB可显著降低脑缺血再灌注损伤 缺血损伤及改善tMCAO后小鼠神经功能缺损。更多 重要的是，我们的实验证明了GB促进了小胶质细胞/巨噬细胞的转移 从炎症M1表型到体内保护性抗炎M2表型 或者体外。血小板活化因子（39f）和血小板活化因子（pa88）沉默 PAF受体参与了小胶质细胞/巨噬细胞极化的调节。 结论：本实验结果揭示了银杏叶提取物的一种新的药理作用 tMCAO后小胶质细胞/巨噬细胞极化，从而加深了我们对tMCAO的认识 银杏叶治疗缺血性中风的神经保护机制。此外，这个新的 这一机制可能允许GB用于其他许多与小胶质细胞/巨噬细胞极化相关的研究 炎症性疾病。

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