rAAV2/1-Acrp30对动脉粥样硬化的GK大鼠NF-κB及黏附分子的影响

Effects of rAAV2/1-Acrp30 on NF-κB and adhesion molecule in GK rats with atherosclerosis

目的观察rAAV2/1-Acrp30对动脉粥样硬化GK大鼠模型血清可溶性细胞间黏附分子(sICAM-1)、可溶性血管内皮黏附分子(sVCAM-1)水平和NF-κB表达的影响,从血管炎症的角度探讨脂联素对糖尿病大血管病变的作用。方法将造模成功的30只动脉粥样硬化的GK大鼠分为三个处理组:①模型1组,后肢肌肉注射盐水;②模型2组,后肢肌肉注射空病毒rAAV2/1;③治疗组,后肢肌肉注射rAAV2/1-Acrp30。治疗8周后处死所有大鼠,比较三组之间血清sICAM-1,sVCAM-1及主动脉处NF-κBp65 mRNA的表达水平。结果治疗组和模型1组、模型2组比较,血清sVCAM-1、sICAM-1显著降低(P<0.05)。治疗组和模型1组、模型2组比较,主动脉NF-κBp65 mRNA表达显著下调(P<0.05)。结论rAAV2/1-Acrp30可通过抑制NF-κB的表达,减轻炎症反应而对糖尿病大血管病变产生保护作用。

Objective To study the effects of rAAV2/1-Acrp30 on sICAM-1 and sVCAM-1 level as well as NF-kB expression in GK rats with diabetic arteriosclerosis so as to explore the effect of adiponectin on diabetic macroangiopathy. Methods A total number of 30 atherosclerotic GK rat models were randomly divided into three groups： ① Model group one （M1） hind limb intramuscular injection of normal saline; ② Model group two （M2） ： hind limb intramuscular injection of vacuity virus rAAV2/1; Q Treatment group （T）： hind limb intramuscular injection of rAAV2/1 -Acrp30 at a dose of 1 × 10n mg/L. After 8 weeks＇ treatment, the rats were killed, and serum sVCAM-1 and sICAM-1 level as well as aortic NF-kBp65mRNA expression were measured in each group. Aortic NF-kBp65mRNA expression was measured by RT-PCR.Results Compared with those in control model groups （M1 and M2）, sVCAM-1 and sICAM-1 levels were decreased significantly in the treatment （T） group （P〈0.05）. Aortic NF-kBp65 mRNA expression was significantly down-regulated in the treatment （T） group compared with that in control model groups （M1 and M2） （P 〈0.05）. Conclusion rAAV2/1-Acrp30 may produce protective effects on diabetic atherosclerosis by decreasing inflammatory reactions.