小檗碱对2型糖尿病大鼠巨噬细胞ox-LDL、CD36和PPARγ的影响

目的探讨小檗碱对T2DM大鼠脂代谢、腹腔巨噬细胞（PM）及肺泡巨噬细胞（AM）氧化低密度脂蛋白（ox-LDL）、CD36和过氧化物酶体增殖物激活受体γ（PPARγ）表达的影响。方法SD大鼠分为正常对照组、高脂组、糖尿病组、小檗碱治疗组。实验结束后测定各组BG、Ins、血脂,PM及AM内ox-LDL含量、CD36与PPARγ的蛋白与mRNA表达水平。结果与正常对照组比较，糖尿病组BG、Ins、TC、TG、LDL-C显著升高；PM及AM内ox-LDL含量、CD36与PPARγ的蛋白和mRNA表达显著升高。与糖尿病组比较，小檗碱治疗组BG、Ins及LDL-C水平降低，TC、TG显著下降，HDL-C升高，PM及AM内ox-LDL含量下降，CD36的蛋白和mRNA表达降低，PPARγ mRNA表达降低。结论小檗碱降低T2DM大鼠血糖，改善胰岛素抵抗和脂代谢紊乱，其机制可能与降低巨噬细胞内ox-LDL，抑制CD36和PPARγ的表达有关。

Effect of berberine treatment on the expressions of oxLDL,CD36 and PPARγ of macrophages from diabetic rats

Objective To study the effect of berberine on the lipid metabolism and the expression of ox-LDL,CD36 and PPARγ in the peritoneal macrophage （PM） and alveolar macrophage （AM） from the type 2 diabetic rats. Methods Sprague-Dauley rats were randomly divided into groups of normal control,high-fat diet, type 2 diabetes and berberine treatment. The levels of blood glucose, insulin and lipid were measured biochemically,the content of ox-LDL in macrophage and the protein expression of CD36 and PPARγ in macrophage were assayed by ELISA, the mRNA expression of CD36 and PPARγ in macrophage was disclosed by RT-PCR. Results Compared with the control group, the levels of glucose,insulin and total cholesterol （TC）,triglycerides（TG）,low density lipoprotein-cholesterol （LDL-C） in blood were in- creased significantly （P〈 0.01）, and high density lipoprotein-cholesterol （HDL-C） was decreased （P 〈0.01） in type 2 diabetic group. The berberine treatment decreased blood glucose, insulin, LDL-C（P〈 0.05） and TC, TG（P〈0. 01） ,but increased the HDL- C level（P〈0.05）. The content of ox-LDL,the protein and mRNA expressions of CD36 and PPARγ in PM and AM increased in type 2 diabetic group（P〈 0. 01） ,while the levels of ox-LDL,the expressions of protein and mRNA of CD36 and PPARγ in PM and AM decreased in berberine treatment group（P〈0.01 or P〈0.05）. Conclusions Berberine may prevent the development of diabetic complication by correcting insulin resistance and ameliorating the disturbance of lipid metabolism. The decreasing of ox-LDL and the inhibiting of the expression of CD36 and PPARy in macrophages may contribute to the prevention.