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目的研究激动κ阿片受体(KOR)对糖尿病大鼠肠系膜小动脉血管舒缩功能及主动脉结构的影响,探讨其作用机制。方法选取雄性SD大鼠40只,分为对照组(16只)和模型组(24只)。其中,对照组分为正常组和正常+U50,488H组(U50,488H 1组),每组8只;模型组分为糖尿病组、糖尿病+U50,488H组(U50,488H 2组)和糖尿病+nor-BNI组(nor-BNI组),每组8只。采用体外血管环灌流技术检测肠系膜小动脉血管舒缩功能;Westernblot法检测小动脉血管组织内皮型一氧化氮合酶(eNOS)、NF-κB及KOR表达水平;光镜HE染色观察主动脉结构变化。结果与正常组比较,糖尿病组对KCl和去甲肾上腺素引起的收缩反应明显增强(P<0.05),对乙酰胆碱引起的舒张反应明显减弱(P<0.05),对硝普钠引起的舒张反应无明显变化;eNOS表达减少,而NF-κB及KOR表达增加(P<0.01)。U50,488H处理后,eNOS及KOR表达增加而NF-κB表达减少;nor-BNI处理后,eNOS及KOR表达减少而NF-κB表达增加(P<0.01)。结论激动KOR可改善糖尿病大鼠肠系膜小动脉血管舒缩功能和主动脉结构,机制可能与通过增加eNOS表达改善内皮功能和通过抑制NF-κB表达降低炎症水平有关。
Objective To investigate the effects of KOR on the vasomotion and aortic structure of mesenteric arterioles in diabetic rats and the possible mechanism. Methods Forty male Sprague-Dawley rats were randomly divided into control group (n = 16) and model group (n = 24). The control group consisted of normal group and normal + U50,488H group (U50,488H1 group), with 8 in each group. The model group consisted of diabetic group, diabetes + U50,488H group (U50,488H2 group) and diabetes + nor-BNI group (nor-BNI group), 8 rats in each group. The vasomotor function of mesenteric arterioles was detected by in vitro vascular perfusion technique. The expression of endothelial nitric oxide synthase (eNOS), NF-κB and KOR were detected by Western blotting. The changes of aortic structures were observed by light microscope (HE staining) . Results Compared with the normal group, the contractile responses to KCl and norepinephrine were significantly increased (P <0.05) and the diastolic responses to acetylcholine (P <0.05) in diabetics were significantly decreased (P <0.05). The diastolic responses to sodium nitroprusside (P <0.01). The expression of NF-κB and KOR were increased (P <0.01). After treatment with nor-BNI, the expression of eNOS and KOR decreased and the expression of NF-κB increased (P <0.01). Conclusion KOR stimulation can improve the vasomotion and aorta structure of mesenteric arterioles in diabetic rats. The mechanism may be related to the enhancement of endothelial function through the increase of eNOS expression and the decrease of inflammation by inhibiting the expression of NF-κB.