6-姜酚降低血管紧张素Ⅱ诱导的血管平滑肌细胞衰老的机制研究

摘要

Objective To investigate the effects of 6‐gingerol on the rat aortic vascular smooth muscle cells (VSMCs)senescence induced by angiotensin Ⅱ(Ang Ⅱ) .Methods Culturing rat VSMCs were stimulated with Ang Ⅱ with or without pretreating with 6‐gingerol .The senescent status of cells was verified by in situ staining for senescence‐associated β‐galactosidase(SA‐β‐gal) .The cell cycle distribution was analyzed by FACS .The protein expression of mTOR and phosphorylated P70‐S6K were detected by Western blot .Results When VSMCs were exposed to AngⅡ ,the senescence marker such as SA‐β‐gal staining and cell cycle arrest‐ing in G0/G1 phage were significantly increased .Furthermore ,the protein level of mTOR ,phosphorylated P70‐S6K were also en‐hanced significantly .However ,6‐gingerol was found to markedly inhibit the senescence‐like phenotype and related signal molecular induced by AngⅡ as mentioned above .Conclusion 6‐gingerol attenuate VSMCs senescence through inhibition of mTOR/P70S6K pathway molecular .%目的：探讨6‐姜酚对血管平滑肌细胞（VSMCs）病理衰老的影响及机制。方法培养的VSMCs细胞，给予血管紧张素Ⅱ（A ng Ⅱ）刺激及6‐姜酚干预，采用β‐半乳糖苷酶染色检测细胞衰老变化，流式细胞术检测细胞周期分布，蛋白免疫印迹法（Western blot）检测mTOR蛋白表达及其底物P70‐S6K磷酸化水平。结果 Ang Ⅱ显著增加VSMCs的β‐半乳糖苷酶染色率、G0/G1期停滞、mTOR蛋白表达及P70‐S6K磷酸化，而6‐姜酚能显著干预上述 Ang Ⅱ诱导的细胞衰老表型及相关信号分子变化。结论6‐姜酚可能通过抑制mTOR/P70‐S6K降低Ang Ⅱ诱导的VSMCs衰老。