Wogonin ameliorates lipotoxicity-induced apoptosis of cultured vascular smooth muscle cells via interfering with DAG-PKC pathway

Aim: To investigate the effects of wogonin (5,7-dihydroxy-8-methoxyflavone) extracted from Scutellaria baicalensis Georgi (S baicalensis) on lipotoxicity-induced apoptosis of vascular smooth muscle cells (VSMCs) and the underlying mechanisms. Methods: Cultured VSMCs were used. Apoptosis of VSMCs was...

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Veröffentlicht in:Acta pharmacologica Sinica 2011-12, Vol.32 (12), p.1475-1482
Hauptverfasser: Liu, Yu-min, Wang, Xiong, Nawaz, Ahmed, Kong, Zhao-hong, Hong, Yan, Wang, Chang-hua, Zhang, Jun-jian
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Sprache:eng
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Zusammenfassung:Aim: To investigate the effects of wogonin (5,7-dihydroxy-8-methoxyflavone) extracted from Scutellaria baicalensis Georgi (S baicalensis) on lipotoxicity-induced apoptosis of vascular smooth muscle cells (VSMCs) and the underlying mechanisms. Methods: Cultured VSMCs were used. Apoptosis of VSMCs was induced by palmitate (0.75 mmoi/L), and detected using TUNEL assay The expression levels of protein and phosphorylated protein were measured using Western blot analysis. Results: Treatment of VSMCs with wogonin (10, 25 and 50 pmol/L) significantly attenuated the apoptosis and endoplasmic reticulum (ER) stress induced by palmitate in concentration- and time-dependent manners. Wogonin (50 pmol/L) decreased palmitate-induced reactive oxygen species (ROS) generation. The ER stress inhibitor 4-phenyl butyric acid (5 mmol/L) significantly decreased palmitate- induced apoptotic cells, and occluded the anti-apoptotic effect of wogonin (25 pmol/L). Wogonin (10, 25 and 50 pmol/L) significantly reduced the intracellular diacylglycerol (DAG) accumulation and expression levels of phosphorylated PKCs in palmitate-treated VSMCs. Conclusion: Our results suggest that wogonin inhibits lipotoxicity-induced apoptosis of VSMCs via suppressing the intracellular DAG accumulation and subsequent inhibition of PKC phosphorylation. Wogonin has therapeutic potential for the prevention and treatment of atherosclerosis.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2011.120