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丹皮酚通过调控血管平滑肌表型转换抑制血管生成。

Paeonol Suppresses Vasculogenesis Through Regulating Vascular Smooth Muscle Phenotypic Switching.

机构信息

College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

College Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

出版信息

J Endovasc Ther. 2022 Feb;29(1):117-131. doi: 10.1177/15266028211032956. Epub 2021 Aug 6.

Abstract

OBJECTIVE

Smooth muscle cell (SMC) phenotypic switching is associated with development of a variety of occlusive vascular diseases. Paeonol has been reported to be involved in suppressing SMC proliferation. However, it is still unknown whether paeonol can regulate SMC phenotypic switching, and which eventually result in suppressing vasculogenesis.

METHODS

Murine left common carotid artery was injured by completely ligation, and paeonol was administrated by intraperitoneal injection. Hematoxylin and eosin (H&E) staining was performed to visualize vascular neointima formation. Rat aortic SMCs were used to determine whether paeonol suppresses cell proliferation and migration. And murine hind limb ischemia model was performed to confirm the function role of paeonol in suppressing vasculogenesis.

RESULTS

Complete ligation of murine common carotid artery successfully induced neointima formation. Paeonol treatment dramatically reduced the size of injury-induced neointima. Using rat aortic primary SMC, we identified that paeonol strongly suppressed cell proliferation, migration, and decreased extracellular matrix deposition. And paeonol treatment dramatically suppressed vasculogenesis after hind limb ischemia injury.

CONCLUSION

Paeonol could regulate SMC phenotypic switching through inhibiting proliferation and migration of SMC, which results in inhibiting ischemia-induced vasculogenesis.

摘要

目的

平滑肌细胞(SMC)表型转换与多种闭塞性血管疾病的发生有关。丹皮酚已被报道参与抑制 SMC 增殖。然而,丹皮酚是否能调节 SMC 表型转换,以及最终抑制血管生成,目前尚不清楚。

方法

通过完全结扎小鼠左颈总动脉造成损伤,腹腔内注射丹皮酚。通过苏木精和伊红(H&E)染色来观察血管新生内膜的形成。使用大鼠主动脉平滑肌细胞(SMC)来确定丹皮酚是否抑制细胞增殖和迁移。并通过小鼠后肢缺血模型来确认丹皮酚在抑制血管生成中的功能作用。

结果

小鼠颈总动脉完全结扎成功诱导了新生内膜的形成。丹皮酚处理显著减少了损伤诱导的新生内膜的大小。使用大鼠主动脉原代 SMC,我们发现丹皮酚强烈抑制细胞增殖、迁移,并减少细胞外基质沉积。丹皮酚处理后,后肢缺血损伤后的血管生成明显受到抑制。

结论

丹皮酚可能通过抑制 SMC 的增殖和迁移来调节 SMC 表型转换,从而抑制缺血诱导的血管生成。

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