糖尿病大鼠肝脏β-defensins表达及血清炎症因子的变化

Expression of β-defensin in liver tissue and alteration of serum inflammatory factors in diabetic rats

目的:观察糖尿病大鼠病程中肝脏β-defensins的表达和血清炎症因子的变化,探讨在糖尿病状态时两者之间可能存在的影响.方法:实验大鼠分为普通饲料组、高糖饲料组、糖尿病4wk组和12wk组,采集血液检测血清炎症因子TNF-α,IL-1β及IL-10和血糖、胰岛素、三酰甘油等相关生化指标;收集肝脏标本,RT-PCR及Western Blot方法检测β-defensins的表达.结果:与对照组相比,糖尿病大鼠整个病程中都存在致炎因子TNF-α,IL-1β激活及抗炎因子IL-10的削弱.肝脏中表达β-defensins1(rBD-1)和β-defensins2(rBD-2).rBD-1呈少量表达,糖尿病病程中rBD-2表达呈减少趋势.高血糖或糖基化反应可能干扰rBD-2的组成性表达及炎症因子产生的诱导性表达.结论:糖尿病大鼠病程中存在慢性炎症,高血糖或糖基化反应干扰了炎症刺激重要的小分子抗菌肽β-defensins在肝脏表达的信号通路,使其表达下调.

AIM： To investigate the expression of β-defensin in liver tissues and alteration of serum inflammatory factors of diabetic rats so as to explore the possible interactive effect. METHODS： SD rats were divided into 4 groups： control group, experimental group, 4 wk diabetic rats group, and 12 wk diabetic rats group. Inflammatory factors of blood serum TNF-α, IL-1β, IL-10 and β-defensin were examined by ELISA method, Western Blot and real time polymerase chain reaction （RT-PCR）. RESULTS： During the whole course of diabetes, there was persistent activation of TNF-α and IL-1 β and ebb of anti-inflammatory factor IL-10. Expression of β-defensinsl （ rBD-1 ） was slight and expression of β-defensins2 （ rBD-2 ） decreased, which suggested that high glucose or glycosylation reaction probably interfered the constitution expression of rBD-2 and reduced the induction expression. CONCLUSION： There exists chronic inflammatory effect significantly in the diabetic liver. As a key role, the impairment of rBD-2 is probably induced by the high glucose and subsequent glycosylation reaction.