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Luteolin Ameliorates Hypertensive Vascular Remodeling through Inhibiting the Proliferation and Migration of Vascular Smooth Muscle Cells

机译:木犀草素通过抑制血管平滑肌细胞的增殖和迁移改善高血压血管的重塑

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摘要

Objectives. Preliminary researches showed that luteolin was used to treat hypertension. However, it is still unclear whether luteolin has effect on the hypertensive complication such as vascular remodeling. The present study was designed to investigate the effect of luteolin on the hypertensive vascular remodeling and its molecular mechanism. Method and Results. We evaluated the effect of luteolin on aorta thickening of hypertension in spontaneous hypertensive rats (SHRs) and found that luteolin could significantly decrease the blood pressure and media thickness of aorta in vivo. Luteolin could inhibit angiotensin II- (Ang II-) induced proliferation and migration of vascular smooth muscle cells (VSMCs). Dichlorofluorescein diacetate (DCFH-DA) staining result showed that luteolin reduced Ang II-stimulated ROS production in VSMCs. Furthermore, western blot and gelatin zymography results showed that luteolin treatment leaded to a decrease in ERK1/2, p-ERK1/2, p-p38, MMP2, and proliferating cell nuclear antigen (PCNA) protein level. Conclusion. These data support that luteolin can ameliorate hypertensive vascular remodeling by inhibiting the proliferation and migration of Ang II-induced VSMCs. Its mechanism is mediated by the regulation of MAPK signaling pathway and the production of ROS.
机译:目标。初步研究表明,木犀草素可用于治疗高血压。然而,目前还不清楚木犀草素是否对高血压并发症如血管重塑有作用。本研究旨在探讨木犀草素对高血压血管重构的影响及其分子机制。方法和结果。我们评估了木犀草素对自发性高血压大鼠(SHRs)高血压主动脉增厚的影响,发现木犀草素可以显着降低体内的血压和主动脉中膜厚度。木犀草素可以抑制血管紧张素II-(Ang II-)诱导的血管平滑肌细胞(VSMCs)增殖和迁移。二乙酸二氯荧光素(DCFH-DA)染色结果表明,木犀草素减少了血管紧张素转换酶中Ang II刺激的ROS产生。此外,蛋白质印迹和明胶酶谱分析结果表明,木犀草素处理导致ERK1 / 2,p-ERK1 / 2,p-p38,MMP2和增殖细胞核抗原(PCNA)蛋白水平降低。结论。这些数据支持木犀草素可以通过抑制Ang II诱导的VSMC的增殖和迁移来改善高血压血管重塑。其机制由MAPK信号传导途径的调节和ROS的产生介导。

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