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目的:改善脂毒性引起的血管内皮细胞损伤在心血管疾病防治中发挥重要作用。本研究旨在探讨叔丁基对苯二酚(tert-butylhydroquinone,TBHQ)对脂毒性引起的血管内皮细胞损伤的保护作用。方法:以人脐静脉血管内皮细胞系EA.hy926为研究对象,给予不同浓度的饱和游离脂肪酸及TBHQ进行干预,检测细胞的凋亡情况。采用westernblotting及信号通路阻断技术对TBHQ的作用机制进行研究。结果:给与血管内皮细胞饱和游离脂肪酸进行干预可显著增加细胞死亡(P<0.05)。TBHQ显著抑制饱和游离脂肪酸诱导的细胞死亡(P<0.05)。激活自噬可显著抑制饱和游离脂肪酸引发的血管内皮细胞脂毒性(P<0.05)。此外,TBHQ可显著激活血管内皮细胞的自噬(P<0.05),采用自噬抑制剂可阻断TBHQ对脂毒性的保护作用(P<0.05)。结论:TBHQ通过激活自噬有效地抑制饱和游离脂肪酸诱导的血管内皮细胞损伤,对于改善或防治高脂血症引起的血管损伤可能具有重要的现实意义。
OBJECTIVE: To improve the lipid peroxidation induced vascular endothelial cell injury plays an important role in the prevention and treatment of cardiovascular diseases. This study aimed to investigate the protective effect of tert-butylhydroquinone (TBHQ) on lipid peroxidation-induced injury of vascular endothelial cells. Methods: Human umbilical vein endothelial cell line EA.hy926 was used as the research object. Different concentrations of saturated free fatty acids and TBHQ were intervened to detect the cell apoptosis. The mechanism of action of TBHQ by westernblotting and signal pathway blocking was studied. Results: Intervention with saturated free fatty acids in vascular endothelial cells significantly increased cell death (P <0.05). TBHQ significantly inhibited cell death induced by saturated free fatty acids (P <0.05). Activation of autophagy significantly inhibited saturated fatty acid-induced vascular endothelial cell lipotoxicity (P <0.05). In addition, TBHQ significantly activated autophagy in vascular endothelial cells (P <0.05). The use of autophagy inhibitors blocked the protective effect of TBHQ on lipotoxicity (P <0.05). CONCLUSION: TBHQ can effectively inhibit the injury of vascular endothelial cells induced by saturated free fatty acids by activating autophagy, which may be of great practical significance for the improvement or prevention of vascular injury caused by hyperlipidemia.