Objective :To examine the changes of regulatory proteins related to inflammation in serum and endothelial cell in obese mice after exercise training and investigate the mechanism of exercise training to improve vascular endothelial function .Methods :Forty SPF C57BL/6 mice were divided randomly into the following three groups :Normal Control group (NC ,n=10) ,sedentary chow diet ,Obese Control group (OC ,n = 10 ) ,high‐fat diet ,Obese Exercise group(OE ,n= 11) ,high‐fat diet ,OE consisted of 8 weeks of 60‐min swimming sessions ,6 days/week .At the end of the training protocol ,Omentin ,TNF‐α ,insulin ,GLU in serum were assayed and the expression of TNF‐α ,AMPK ,eNOS in endothelial cell was observed both at the mRNA level and the protein level by the methods of RT‐PCR and immunohistochemistry , respectively .Meanwhile ,the structure of aortic endothelial cells was observed by transmission electron microscopy .Results :1) The serum Omentin in OC was significantly lower than NC (P<0 .01);as well as the OE group significantly increased the serum Omentin ,compared with OC(P< 0 .01);the serum TNF‐α ,GLU ,Insulin levels in OC group were significantly higher than OE group(P< 0 .01) .However ,they are lower in OE than in OC .2) Serum Omentin levels are negatively correlated with abdominal fat weight (r= 0 .72 ,P<0 .01) ,serum TNF‐α( r= -0 .63 ,P< 0 .01 ) ,index of insulin resistance ( r= -0 .64 ,P< 0 .01 ) .3 ) Compared with the NC group ,the expression of thoracic aorta AMPK ,eNOS in OC were significantly lower(P< 0 .01);Compared with the OC group ,OE mice thoracic aorta AMPK ,eNOS ex‐pression increased(P< 0 .01);4) The endothelial cells and the sub endothelial structure of aortic endothelium in OC group showed pathologic changes .8‐week swimming exercise makes the thoracic aorta morphology improved in OE group mice .Conclusion :8‐week swimming exer‐cise can effectively reduce weight ,decrease chronic inflammation and alleviate injury of vascular endothelial cell in obese mice ,inhibition of inflammation may be one of the important mecha‐nisms of exercise improving endothelial dysfunction related to obesity .%目的：通过研究运动干预后肥胖小鼠血液、血管内皮致炎和抗炎相关细胞因子的水平及相关调控蛋白表达的变化，从运动抗炎症的角度揭示运动改善肥胖相关血管内皮功能障碍的机制。方法：SPF级雄性断乳 C57BL／6小鼠40只，随机分为正常对照组（NC ，n＝10）、肥胖对照组（OC ，n＝10）和肥胖运动干预组（OE ，n＝11），采用高脂饮食诱导肥胖模型后，对OE组小鼠进行8周游泳运动干预（6次／周，60min／次）。运动干预后检测小鼠血清网膜素（Omentin）、肿瘤坏死因子‐α（TNF‐α）、胰岛素（Insulin）、空腹血糖（GLU ）；并采用免疫组化及RT‐PCR技术检测主动脉内皮AMPK、TNF‐α、eNOS的蛋白及mRNA表达，透射电镜观察小鼠主动脉内皮细胞的形态学改变。结果：1）与NC比较，OC小鼠血清Omentin水平显著降低（ P＜0．01）；与OC比较，OE小鼠血清 Omentin水平上升，差异显著（ P＜0．01）；此外，与NC比较，OC小鼠血清 TNF‐α、GLU、Insulin显著升高（P＜0．01），而与OC比较，OE小鼠上述指标显著降低（ P＜0．01）。2）血清 Omentin水平与体重（ r＝－0．69，P＜0．01）、血清TNF‐α（r＝－0．63，P＜0．01）、胰岛素抵抗指数（r＝－0．64，P＜0．01）均呈负相关关系。3）与NC比较，OC 小鼠主动脉 AMPK、eNOS 表达降低（ P＜0．01），TNF‐α表达上调（ P＜0．01）；与OC相比，OE小鼠主动脉 AMPK、eNOS表达上调（P＜0．01），TNF‐α表达下降（P＜0．01）。4）OC小鼠存在主动脉内皮细胞损伤，而 OE小鼠主动脉内皮细胞损伤得到缓解。结论：8周游泳运动干预可有效降低肥胖小鼠体重，减轻慢性炎症反应，缓解血管内皮细胞损伤；运动抑制炎症反应可能是其改善肥胖相关血管内皮功能障碍的重要机制之一。
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