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目的研究阿托伐他汀对链脲佐菌素(STZ)诱导的I型糖尿病大鼠炎性反应的影响。方法8周龄SD雄性大鼠2次腹腔注射STZ诱发实验性I型糖尿病,以不足以产生降血脂作用的小剂量阿托伐他汀对糖尿病大鼠进行干预,检测空腹血糖、血清甘油三酯、总胆固醇、低密度和高密度脂蛋白、肿瘤坏死因子-α(TNF-α)、C-反应蛋白(CRP)及白细胞介素1β(IL-1β)的水平,并观察主动脉壁组织中TNF-α、IL-1β、血管粘附分子-1(VCAM-1)、胞间粘附分子-1(ICAM-1)mRNA的表达。结果实验性I型糖尿病大鼠血中TNF-α、CRP、IL-1β水平分别为(2.118±0.153)μg/L、(2.857±1.032)mg/L和(0.2347±0.1264)μg/L,均高于无糖尿病大鼠对照组(P<0.05)。主动脉壁组织中的TNF-α、IL-1β、VCAM-1、ICAM-1mRNA的表达上调(P<0.05)。糖尿病大鼠阿托伐他汀干预组血中TNF-α、CRP、IL-1β水平分别为(1.602±0.145)μg/L,(2.263±0.691)mg/L和(0.1565±0.037)μg/L,均低于糖尿病大鼠对照组(P<0.05)。主动脉壁组织中的TNF-α、IL-1β、VCAM-1、ICAM-1mRNA的表达下调(P<0.05)。结论低剂量阿托伐他汀能抑制链脲佐菌素诱导的I型糖尿病大鼠炎性反应,其机制与阿托伐他汀降血脂作用无关。
Objective To investigate the effect of atorvastatin on the inflammatory response in streptozotocin (STZ) -induced type 1 diabetic rats. Methods SD male rats of 8 weeks old were injected intraperitoneally twice with STZ to induce experimental type I diabetes mellitus. Small doses of atorvastatin not enough to produce hypolipidemic effect were used to interfere diabetic rats. Fasting plasma glucose, serum triglyceride, Total cholesterol, low density and high density lipoprotein, tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) and interleukin 1β (IL-1β) α, IL-1β, VCAM-1 and ICAM-1 mRNA were detected by ELISA. Results The levels of TNF-α, CRP and IL-1β in blood of experimental type I diabetic rats were (2.118 ± 0.153) μg / L, (2.857 ± 1.032) mg / L and Higher than the control group without diabetes (P <0.05). The expressions of TNF-α, IL-1β, VCAM-1 and ICAM-1 mRNA in the aortic wall tissue were up-regulated (P <0.05). The level of TNF-α, CRP and IL-1β in atorvastatin group were (1.602 ± 0.145) μg / L, (2.263 ± 0.691) mg / L and (0.1565 ± 0.037) μg / L respectively in diabetic rats, Were lower than the diabetic rats control group (P <0.05). The expressions of TNF-α, IL-1β, VCAM-1 and ICAM-1 mRNA in the aortic wall tissue were down-regulated (P <0.05). Conclusions Low-dose atorvastatin can inhibit streptozotocin-induced inflammatory response in type 1 diabetic rats. The mechanism of atorvastatin is not related to the lipid-lowering effect of atorvastatin.