Objectives

Following stroke, angiogenic strategy has been proposed to alleviate ischemia-induced injury by promoting angiogenesis and improving cerebrovascular function in the ischemic regions. Ligustilide (LGSL) is known to have neuroprotection against ischemic stroke-induced injury. But the effect of LGSL on promoting angiogenesis after ischemic stroke is unknown. The purpose of this study was to determine the effects of LGSL on neuroprotection and angiogenesis after stroke.

Methods

BrdU cell proliferation assay, transwell, wound healing, and tube-formation experiments were performed to evaluate the effects of LGSL on mouse microvascular endothelial cells (bEnd.3). Male adult C57/BL6 mice were subjected to focal transient cerebral ischemia followed by intragastric LGSL administration. Immunostaining was performed to assess angiogenesis. VEGF level was assayed by ELISA. eNOS expression was performed by Western blot.

Results

LGSL significantly improved neurological function. LGSL promoted angiogenesis in vitro and in vivo. Neurological improvement conferred by LGSL correlated with increased cerebral vessels number. We also found an increase of VEGF and eNOS activation in mice ischemic hemisphere following LGSL administration.

Conclusion

LGSL promoted focal angiogenesis and attenuated ischemia-induced brain injury, suggesting that LGSL is a potential agent that improves angiogenesis and promotes recovery from ischemic stroke.

中文翻译：

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gust本内酯通过促进脑缺血后的血管生成来提供神经保护作用。

目标

中风后，已经提出了通过在缺血区域促进血管生成和改善脑血管功能来减轻缺血引起的损伤的血管生成策略。已知本内酯（LGSL）对缺血性中风诱发的损伤具有神经保护作用。但是，LGSL促进缺血性中风后促进血管生成的作用尚不清楚。这项研究的目的是确定LGSL对中风后神经保护和血管生成的影响。

方法

进行BrdU细胞增殖测定，转运，伤口愈合和管形成实验以评估LGSL对小鼠微血管内皮细胞的影响（bEnd.3）。对雄性成年C57 / BL6小鼠进行局灶性短暂性脑缺血，然后给予胃内LGSL。进行免疫染色以评估血管生成。通过ELISA测定VEGF水平。通过蛋白质印迹进行eNOS表达。

结果

LGSL明显改善了神经功能。LGSL促进血管生成的体外和体内。LGSL带来的神经功能改善与脑血管数目增加有关。我们还发现LGSL给药后，小鼠缺血性半球中VEGF和eNOS的激活增加。

结论

LGSL促进局灶性血管生成并减轻局部缺血引起的脑损伤，这表明LGSL是改善血管生成并促进缺血性中风恢复的潜在药物。