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目的探讨阿托伐他汀对胰岛素抵抗大鼠心肌肥厚的影响及其机制。方法雄性SD大鼠45只随机分为三组(对照组、果糖组以及果糖加阿托伐他汀组),每组15只,其中果糖组给予10%果糖水诱导胰岛素抵抗,果糖加阿托伐他汀组给予30 mg/d阿托伐他汀灌胃以及10%果糖水,对照组大鼠不给予果糖水和阿托伐他汀,连续处理56 d,OGTT评定胰岛素敏感性,心肌HE染色评定心肌肥厚,放免法测定血管紧张素Ⅱ,Western blot测定心肌ATⅡ表达水平。结果 (1)OGTT显示果糖组与对照组相比血糖显著升高[(6.41±0.57)mmol/L vs.(4.01±0.23)mmol/L,P<0.01]及胰岛素变化[(29.42±1.87)nIU vs.(9.30±1.54)nIU,P<0.01]显著升高,而果糖加阿托伐他汀组较果糖组血糖[(4.30±0.62)mmol/L vs.(6.41±0.57)mmol/L,P<0.05]以及胰岛素[(9.30±1.54)nIU vs.(29.42±1.87)nIU,P<0.01]显著下降显著下降;(2)果糖组心肌HE染色显示左心室肥厚,而果糖加阿托伐他汀组与对照组无显著变化;(3)果糖组与对照组以及果糖加阿托伐他汀组相比血管紧张素Ⅱ水平显著升高[(3.95±0.20)mmol/L vs.(2.84±0.18)mmol/L,P<0.01;(3.95±0.20)mmol/L vs.(3.01±0.25)mmol/L,P<0.01]显著升高,而其余两组相比无统计学差异;(4)果糖组ATⅡ表达相对百分比较对照组以及果糖加阿托伐他汀组显著增加(1.99 vs.1.00,P<0.01;1.99 vs.0.98,P<0.01);而其余两组相比无统计学差异。结论阿托伐他汀可改善胰岛素抵抗所导致的心肌肥厚,这可能与阿托伐他汀改善胰岛素敏感性、降低血浆血管紧张素Ⅱ以及降低心肌细胞血管紧张素受体ATⅡ表达有关。
Objective To investigate the effect of atorvastatin on cardiac hypertrophy in insulin resistance rats and its mechanism. Methods 45 male SD rats were randomly divided into three groups (control group, fructose group and fructose plus atorvastatin group), with 15 rats in each group. Fructose group was given 10% fructose water to induce insulin resistance, fructose and atorvastatin The rats in the statin group were given 30 mg / day atorvastatin and 10% fructose water. The rats in the control group were given fructose and atorvastatin continuously for 56 days. OGTT was used to evaluate the insulin sensitivity. The myocardial hypertrophy , Radioimmunoassay of angiotensin Ⅱ, Western blot determination of myocardial AT Ⅱ expression levels. Results (1) OGTT showed that compared with the control group, the blood sugar of fructose group was significantly higher than that of the control group [(6.41 ± 0.57) mmol / L vs. (4.01 ± 0.23) mmol / L, P <0.01] and [29.42 ± 1.87 (4.30 ± 0.62) mmol / L vs. (6.41 ± 0.57) mmol / L for fructose plus atorvastatin group compared with that of fructose group [nIU vs. (9.30 ± 1.54) nIU, P <0.01] P <0.05] and insulin [(9.30 ± 1.54) nIU vs. (29.42 ± 1.87) nIU, P <0.01]; (2) HE staining of left ventricular hypertrophy in fructose group, (3) The level of angiotensin Ⅱ in fructose group was significantly higher than that in control group and fructose plus atorvastatin group [(3.95 ± 0.20) mmol / L vs. (2.84 ± 0.18 ) (P <0.01); (3.95 ± 0.20) mmol / L vs. (3.01 ± 0.25) mmol / L, P <0.01], while there was no significant difference between the other two groups; The relative percentage of ATⅡ expression in fructose group was significantly higher than that in control group and fructose plus atorvastatin group (1.99 vs.1.00, P <0.01; 1.99 vs.0.98, P <0.01), while there was no significant difference between the other two groups. Conclusions Atorvastatin can improve myocardial hypertrophy induced by insulin resistance, which may be related to atorvastatin to improve insulin sensitivity, reduce plasma angiotensin Ⅱ and reduce myocardial angiotensin receptor AT Ⅱ expression.