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目的观察不同时相使用阿托伐他汀对血管内皮细胞自噬的影响,探讨其保护血管内皮细胞的可能机制。方法用Hanks’液替代培养基进行饥饿诱导血管内皮细胞发生自噬的方法。分别在诱导自噬前和诱导过程中,使细胞分别与含或不含阿托伐他汀的正常培养基或Hanks’液共孵育,RT-PCR技术检测组间Beclin-1和Map1lc3两基因的表达。结果与空白对照组相比,诱导前和诱导中都应用阿托伐他汀组和仅在诱导中应用阿托伐他汀组的Beclin-1和Map1lc3两基因mRNA表达均明显降低(P<0.01)。诱导前应用阿托伐他汀组的表达低于对照组,但无统计学意义(P>0.05)。诱导前和诱导中都应用阿托伐他汀组的表达低于仅在诱导中应用阿托伐他汀组,但无统计学意义(P>0.05)。结论阿托伐他汀可以抑制血管内皮细胞自体吞噬,这一作用可能与阿托伐他汀改善血管内皮功能的机制有关。
Objective To observe the effect of atorvastatin on the autophagy of vascular endothelial cells in different phases and to explore its possible mechanism of protecting vascular endothelial cells. Methods Hanks’ solution was used instead of medium to induce starvation induced autophagy in vascular endothelial cells. The cells were respectively co-incubated with normal saline or Hanks’ solution, with or without atorvastatin, before and during the induction of autophagy. The expression of Beclin-1 and Map1lc3 genes were detected by RT-PCR . Results Compared with the blank control group, mRNA expression of Beclin-1 and Map1lc3 both in atorvastatin group and atorvastatin group before induction were significantly decreased (P <0.01). Before induction, the expression of atorvastatin group was lower than that of the control group, but there was no statistical significance (P> 0.05). The expression of atorvastatin group before induction and induction was lower than that of atorvastatin only induction, but not statistically significant (P> 0.05). Conclusions Atorvastatin can inhibit the autophagy of vascular endothelial cells, which may be related to the mechanism of atorvastatin in improving vascular endothelial function.