缺血性脑血管病细胞自噬相关因子与斑块炎性反应的相关性

目的 探讨缺血性脑血管患者细胞自噬相关因子与炎性因子的相关性,为完善其病理机制,寻找新的治疗靶点提供依据.方法 选取缺血性脑血管病患者85例,按照颈动脉斑块分级分为三组:Ⅰ级21例、Ⅱ级35例、Ⅲ级29例,并以33例健康志愿者为对照组.抽取空腹肘静脉血,采用WB法测定自噬相关因子LC3-Ⅱ/LC3-Ⅰ与Beclin-1的蛋白表达量,采用ELISA法测定炎性因子IL-1β、IL-6和TNF-α水平.结果 对照组、Ⅰ级斑块、Ⅱ级斑块、Ⅲ级斑块的LC3-Ⅱ/LC3-Ⅰ、Beclin1表达和血清IL-1β、IL-6和TNF-α水平依次升高(P<0.05);经Pearson分析,LC3-Ⅱ/LC3-Ⅰ表达与IL-1β、IL-6和TNF-α水平之间,Beclin1表达与IL-1β、IL-6和TNF-α水平之间均呈线性正相关(P<0.05);经秩相关分析,颈动脉斑块分级与LC3-Ⅱ/LC3-Ⅰ、IL-1β、IL-6、TNF-α之间均呈正相关性(P<0.05).结论 缺血性脑血管病患者细胞自噬能够通过与炎性反应的相互作用影响斑块稳定性,可能为其病理机制的重要组成部分.

Correlation of autophagy related factors to plaque inflammatoryreaction in patients with ischemic cerebrovascular diseases

Objective To understand the correlation of autophagy related factors and plaque inflammatory reaction in patients with ischemic cerebrovascular diseases so as to obtain scientific knowledge for the development of a more effective method for treating the diseases.Method 85 patients with ischemic cerebrovascular disease were firstly chosen as the subjects of study and divided into 3 groups according to carotid plague degree: Degree 1 (n=21), Degree 2 (n=35), Degree 3 (n=29), and then 33 healthy volunteers were chosen as the control group.The fasting venous blood was extracted to detect LC3-Ⅱ/LC3-Ⅰ and Beclin 1 expression by WB assay, and to detect serum levels of IL-1β、IL-6 and TNF-α by ELISA assay.Findings There was significant difference in LC3-Ⅱ/LC3-Ⅰand Beclin 1 expression, and serum IL-1β, IL-6, TNF-α levels (P<0.05).The LSD-t test results showed that all the indexes increased in the control group and the experimental groups, namely, Degree 1, Degree 2, and Degree 3.There was significant difference between the groups (P<0.05).The Pearson analysis results showed that both LC3-Ⅱ/ LC3-Ⅰ expression and Beclin1 expression had linear positive correlation with serum IL-1β, IL-6, TNF-α levels (P<0.05).Conclusion In ischemic cerebrovascular diseases, autophagy related factors influence plaque stability by interacting with inflammatory reaction factors, which may be an important component of the pathomechanism.