论文部分内容阅读
目的探讨白藜芦醇在动脉粥样硬化(AS)进展中的作用和机制。方法 ApoE~(-/-)小鼠60只随机分为4组(每组15只):对照组、高脂喂养组、白藜芦醇组、高脂喂养+白藜芦醇组。HE染色法观察主动脉斑块病理学改变,生化分析仪检测血脂变化,蛋白质免疫印迹方法(Western blot)测定血管组织微管相关蛋白1轻链3(LC3)以及自噬相关蛋白p62变化。体外培养小鼠巨噬细胞RAW264.7,随机分为4组:对照组、氧化低密度脂蛋白(ox-LDL)损伤组、白藜芦醇组、ox-LDL损伤+白藜芦醇组。TUNEL法检测细胞凋亡,蛋白质Western blot测定自噬相关蛋白LC3Ⅱ、p62的表达。结果与高脂喂养组比较,白藜芦醇干预后,AS斑块面积减少(P<0.05),LC3Ⅱ水平上调(P<0.05),p62水平下降(P<0.05),表明白藜芦醇可以诱导自噬;同样,与ox-LDL损伤组比较,白藜芦醇干预后,损伤的巨噬细胞中凋亡水平下降(P<0.05),LC3Ⅱ水平升高(P<0.05),p62水平下降(P<0.05)。结论 AS进展中会伴随自噬水平的下降,给予白藜芦醇处理后,能够延缓AS进展,其机制可能与白藜芦醇调节自噬能力有关。
Objective To investigate the role and mechanism of resveratrol in the progression of atherosclerosis (AS). Methods Sixty ApoE ~ (- / -) mice were randomly divided into 4 groups (15 in each group): control group, high fat diet group, resveratrol group, high fat diet + resveratrol group. The pathological changes of aortic plaque were observed by HE staining. The changes of serum lipids were detected by biochemical analyzer. The changes of LC3 and p62 protein were detected by Western blot. RAW264.7 cells were cultured in vitro and randomly divided into 4 groups: control group, ox-LDL injury group, resveratrol group, ox-LDL injury + resveratrol group. Apoptosis was detected by TUNEL method and the expression of autophagy-related proteins LC3 Ⅱ and p62 were detected by Western blot. Results Compared with the high fat diet group, the area of AS plaque decreased (P <0.05), the level of LC3 Ⅱ increased (P <0.05) and the level of p62 decreased (P <0.05) after resveratrol treatment, indicating that resveratrol can (P <0.05), while the level of LC3Ⅱ increased (P <0.05) and the level of p62 decreased after resveratrol treatment, compared with the ox-LDL group (P <0.05). Conclusions The progress of AS is accompanied with the decrease of autophagy. Resveratrol can delay the progression of AS. The mechanism may be related to the regulation of autophagy by resveratrol.