乙醇通过抑制NLRP3炎性小体减轻冠状动脉粥样硬化  

Ethanol inhibiting the NLRP3 inflammasome activation to protect coronary heart disease

作　　者：周婧[1] 姜迎萍[1] 赵一俏[2] 

机构地区：[1]广东省第二人民医院康复医学科,广州市510120 [2]广东省第二人民医院心血管内科,广州市510120

出　　处：《实用医学杂志》2016年第19期3164-3167,共4页The Journal of Practical Medicine

摘　　要：目的：探讨乙醇是否通过参与调节培养的人巨噬细胞细胞内白介素1α（IL-1α）的分泌过程，从而发挥对冠状动脉心脏疾病的保护作用。方法：培养人的人单核巨噬细胞系（THP-1）至2-3代后，加入佛波酯（PMA）孵育72 h 诱导THP-1细胞分化为巨噬细胞。用ELIAS 方法检测脂多糖（LPS）、胆固醇（CHOL）及乙醇（ethanal）对巨噬细胞分泌IL-1α的影响。结合ELISA结果，用Western blot 方法检测乙醇对Caspase-1、NLRP3蛋白表达情况。结果：与空白对照组相比，LPS组及LPS ＋ CHOL组IL-1α的浓度升高。与LPS ＋CHOL 组比较，LPS ＋ CHOL ＋ etha 组 IL-1α的浓度显著下降（P ＜0．01）。 Western blot 结果显示乙醇抑制Caspase-1、NLRP3蛋白激活。结论：乙醇抑制巨噬细胞中NLRP3炎性小体激活可能是适度饮酒对冠状动脉心脏疾病的潜在保护作用的生物学途径。Objective To examine whether ethanol modulates the intracellular processes involved in the secretion of IL-1α,and then exert a protective effect against coronary heart disease. Methods THP-1 cells in human were cultured for 2-3 generations , and put in PMF for 72 h to induce THP-1 into macrophage. ELISA was applied to detect effects for secretion of IL-1α by LPS, cholesterol and ethanol. In the light of ELISA re-sults, western blot was applied to detect the effects of ethanol on caspase-1 and NLRP3. Results Compared with the control group, the secretion of IL-1α in LPS group and LPS ＋ CHOL group increased. Compared withLPS ＋ CHOL group, the concentration of IL -1α in LPS ＋ CHOL ＋ etha group significantly decrease（P 〈 0.01）. The results of western blot showed that ethanol significantly inhibited caspase-1 and NLRP3 activation. Conclu-sion Ethanol can inhibit the NLRP3 inflammasome activation in macrophages , which may represent a biological pathway underlying the protective effect of moderate alcohol consumption on coronary heart disease.

关 键 词：冠状动脉粥样硬化 乙醇 IL-1Α NLRP3 

分 类 号：R543.5[医药卫生—心血管疾病]