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衰老大鼠长期补充辅酶Q10后动脉张力的控制

Control of arterial tone after long-term coenzyme Q10 supplementation in senescent rats.

作者信息

Lönnrot K, Pörsti I, Alho H, Wu X, Hervonen A, Tolvanen J P

机构信息

Laboratory of Neurobiology, University of Tampere, Medical School, Finland.

出版信息

Br J Pharmacol. 1998 Aug;124(7):1500-6. doi: 10.1038/sj.bjp.0701970.

Abstract
  1. Age-associated deterioration of arterial function may result from long-lasting oxidative stress. Since coenzyme Q (Q10) has been suggested to protect the vascular endothelium from free radical-induced damage, we investigated the effects of long-term dietary Q10 supplementation on arterial function in senescent Wistar rats. 2. At 16 months of age, 18 rats were divided into two groups. The control group was kept on a standard diet while the other group was supplemented with Q10 (10 mg kg(-1) day(-1)). In addition, nine rats (age 2 months) also ingesting a standard diet were used as the young control group. After 8 study weeks the responses of the mesenteric arterial rings in vitro were examined. 3. Endothelium-independent arterial relaxations to isoprenaline and nitroprusside (SNP) were attenuated in aged rats. Increased dietary Q10 clearly enhanced the relaxation to isoprenaline, but did not affect the response to SNP. In addition, vasodilation of noradrenaline-precontracted rings to acetylcholine (ACh), which was also impaired in aged vessels, was improved after Q10 supplementation. Cyclooxygenase inhibition with diclofenac enhanced the relaxation to ACh only in young rats, while it abolished the difference between the old controls and Q10 supplemented rats, suggesting that the improved endothelium-dependent vasodilation observed in Q10 supplemented rats was largely mediated by prostacyclin (PGI2). 4. In conclusion, long-term Q10 supplementation improved endothelium-dependent vasodilation and enhanced beta-adrenoceptor-mediated arterial relaxation in senescent Wistar rats. The mechanisms underlying the improvement of endothelial function may have included augmented endothelial production of PGI2, increased sensitivity of smooth muscle to PGI2, or both.
摘要
  1. 动脉功能随年龄增长而恶化可能是长期氧化应激所致。由于辅酶Q(Q10)被认为可保护血管内皮免受自由基诱导的损伤,我们研究了长期膳食补充Q10对衰老Wistar大鼠动脉功能的影响。2. 16月龄时,将18只大鼠分为两组。对照组维持标准饮食,另一组补充Q10(10 mg·kg⁻¹·天⁻¹)。此外,9只2月龄且同样摄入标准饮食的大鼠作为年轻对照组。8周研究期后,检测肠系膜动脉环的体外反应。3. 老龄大鼠对异丙肾上腺素和硝普钠(SNP)的非内皮依赖性动脉舒张减弱。增加膳食Q10摄入量明显增强了对异丙肾上腺素的舒张作用,但不影响对SNP的反应。此外,老龄血管中去甲肾上腺素预收缩环对乙酰胆碱(ACh)的血管舒张功能受损,补充Q10后有所改善。双氯芬酸抑制环氧化酶仅在年轻大鼠中增强了对ACh的舒张作用,而消除了老龄对照组和补充Q10大鼠之间的差异,这表明在补充Q10的大鼠中观察到的内皮依赖性血管舒张改善很大程度上是由前列环素(PGI2)介导的。4. 总之,长期补充Q10可改善衰老Wistar大鼠的内皮依赖性血管舒张,并增强β-肾上腺素能受体介导的动脉舒张。内皮功能改善的潜在机制可能包括内皮PGI2生成增加、平滑肌对PGI2的敏感性增加,或两者兼有。

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