论文部分内容阅读
目的探讨护心方抗动脉粥样硬化的可能作用机制。方法用160 nmol/L佛波醇酯类多克隆刺激剂孵育THP-1细胞24 h后诱导分化成巨噬细胞,加入50 mg/L氧化低密度脂蛋白(ox-LDL)培养48 h,使其转化为泡沫细胞。以40%护心方含药血清作用12 h。采用蛋白质印迹检测自噬相关蛋白微管相关蛋白轻链3Ⅱ(LC3-Ⅱ)、微管相关蛋白轻链3I(LC3-Ⅰ)、Beclin-1及p62表达,激光共聚焦显微镜观察自噬蛋白指标LC3B在细胞内分布及含量。结果与空白组比较,模型组LC3-Ⅱ/LC3-Ⅰ和Beclin-1表达显著增加,p62表达显著降低,LC3B表达平均荧光强度显著升高(P<0.05);与模型组比较,护心方组LC3-Ⅱ/LC3-Ⅰ和Beclin-1表达显著降低,p62表达显著升高,LC3B表达平均荧光强度降低(P<0.05)。结论护心方能够逆转ox-LDL诱导的细胞自噬相关蛋白的表达,从而抵抗动脉硬化过程中过度自噬。这可能是其抗动脉粥样硬化的机制之一。
Objective To investigate the possible mechanism of Huoxin Decoction against atherosclerosis. Methods THP-1 cells were incubated with 160 nmol / L phorbol ester polyclonal agonist for 24 h and then induced to differentiate into macrophages. The cells were cultured for 48 h with 50 mg / L ox-LDL It is transformed into foam cells. Forty percent care heart containing serum 12 h. Western blotting was used to detect the expression of LC3-Ⅱ, LC3-Ⅰ, Beclin-1 and p62 in autophagy-related protein microtubule-associated proteins. The expression of autophagy was detected by laser confocal microscopy LC3B in the cell distribution and content. Results Compared with the blank group, the expressions of LC3-Ⅱ / LC3-Ⅰ and Beclin-1 in the model group were significantly increased, the expression of p62 was significantly decreased and the average fluorescence intensity of LC3B expression was significantly increased (P <0.05). Compared with the model group, The expression of LC3-Ⅱ / LC3-Ⅰ and Beclin-1 were significantly decreased, the expression of p62 was significantly increased and the average fluorescence intensity of LC3B was decreased (P <0.05). Conclusion Huoxin Recipe can reverse the expression of autophagy-related protein induced by ox-LDL and thus resist excessive autophagy during atherosclerosis. This may be one of its anti-atherosclerotic mechanisms.