Ginkgolide K (GK) is a new compound extracted from the leaves of Ginkg的简体中文翻译

Ginkgolide K (GK) is a new compound

Ginkgolide K (GK) is a new compound extracted from the leaves of Ginkgo biloba, which has been recognized toexert anti-oxidative stress and neuroprotective effect on ischemic stroke. While whether it plays an enhancedeffect on angiogenesis during ischemic stroke remains unknown. The aim of this study was to investigate theeffect of ginkgolide K on promoting angiogenesis as well as the protective mechanism after cerebral ischemiareperfusion.Using the transient middle cerebral artery occlusion (tMCAO) mouse model, we found that GK (3.5,7.0, 14.0 mg/kg, i.p., bid., 2 weeks) attenuated neurological impairments, and promoted angiogenesis of injuredipsilateral cortex and striatum after 14 days of cerebral ischemia-reperfusion in mice. Further, GK (3.5 mg/kg invivo, 10 μM in vitro) significantly up-regulated the expressions of HIF-1α and VEGF in tMCAO mouse brains andin b End3 cells after OGD/R, and GK-induced upregulation of HIF-1α and VEGF in b End3 cells could beabolished by JAK2/STAT3 inhibitor AG490. Our results demonstrate that GK promotes angiogenesis afterischemia stroke through increasing the expression of HIF-1α/VEGF via JAK2/STAT3 pathway, which provide aninsight into the novel clinical application of GK and its analogs in ischemic stroke therapy in future.
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银杏内酯K(GK)是从银杏叶片中提取的一种新化合物,已被公认<br>对缺血性中风具有抗氧化作用和神经保护作用。虽然它是否<br>在缺血性中风期间对血管生成具有增强作用尚不清楚。本研究的目的是研究<br>银杏内酯K对促进脑缺血再灌注后血管新生的保护作用及其机制。<br>使用短暂的大脑中动脉闭塞(tMCAO)小鼠模型,我们发现GK(<br>3.5、7.0、14.0 mg / kg,腹膜内,腹腔注射,2周)减轻了神经功能障碍,并促进了<br>14岁后同侧皮层和纹状体受损的血管生成小鼠脑缺血再灌注的天数。此外,GK(3.5 mg / kg<br>体内,体外10μM)可显着上调<br>OGD / R后tMCAO 小鼠脑和b End3细胞中HIF-1α和VEGF的表达,而GK诱导b End3细胞中HIF-1α和VEGF的上调可能是由于<br>被JAK2 / STAT3抑制剂AG490废除。我们的结果表明,GK可<br>通过JAK2 / STAT3途径增加HIF-1α/ VEGF的表达,从而促进缺血性卒中后的血管生成,从而为<br>将来在缺血性卒中治疗中GK及其类似物的新型临床应用提供了见识。
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结果 (简体中文) 2:[复制]
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Ginkgolide K (GK) is a new compound extracted from the leaves of Ginkgo biloba, which has been recognized to<br>exert anti-oxidative stress and neuroprotective effect on ischemic stroke. While whether it plays an enhanced<br>effect on angiogenesis during ischemic stroke remains unknown. The aim of this study was to investigate the<br>effect of ginkgolide K on promoting angiogenesis as well as the protective mechanism after cerebral ischemiareperfusion.<br>Using the transient middle cerebral artery occlusion (tMCAO) mouse model, we found that GK (3.5,<br>7.0, 14.0 mg/kg, i.p., bid., 2 weeks) attenuated neurological impairments, and promoted angiogenesis of injured<br>ipsilateral cortex and striatum after 14 days of cerebral ischemia-reperfusion in mice. Further, GK (3.5 mg/kg in<br>vivo, 10 μM in vitro) significantly up-regulated the expressions of HIF-1α and VEGF in tMCAO mouse brains and<br>in b End3 cells after OGD/R, and GK-induced upregulation of HIF-1α and VEGF in b End3 cells could be<br>abolished by JAK2/STAT3 inhibitor AG490. Our results demonstrate that GK promotes angiogenesis after<br>ischemia stroke through increasing the expression of HIF-1α/VEGF via JAK2/STAT3 pathway, which provide an<br>insight into the novel clinical application of GK and its analogs in ischemic stroke therapy in future.
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结果 (简体中文) 3:[复制]
复制成功!
银杏内酯K(Ginkgolide K,GK)是从银杏叶中提取的一种新化合物<br>发挥抗氧化应激和神经保护作用。而它是否发挥了增强<br>缺血性卒中对血管生成的影响尚不清楚。本研究的目的是调查<br>银杏内酯K促进脑缺血再灌注后血管生成的作用及保护机制。<br>采用短暂性大脑中动脉闭塞(tMCAO)小鼠模型,我们发现GK(3.5,0.5,0.0±0.0)的小鼠脑缺血再灌注模型,<br>7.0,14.0 mg/kg,静脉滴注,2周)可减轻神经损伤,促进损伤血管新生<br>小鼠脑缺血再灌注14天后同侧皮质和纹状体。此外,GK(3.5 mg/kg英寸<br>HIF-1α和VEGF在tMCAO小鼠脑组织中的表达显著上调<br>OGD/R后b端3细胞HIF-1α和VEGF的上调可能与GK诱导的b端3细胞HIF-1α和VEGF表达有关<br>被JAK2/STAT3抑制剂AG490废除。我们的结果表明,GK促进血管生成<br>通过JAK2/STAT3途径增加HIF-1α/VEGF的表达,从而提供<br>展望未来GK及其类似物在缺血性脑卒中治疗中的新临床应用。<br>
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