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首页> 外文期刊>Therapeutic advances in cardiovascular disease. >Sesamin enhances nitric oxide bioactivity in aortas of spontaneously hypertensive rats
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Sesamin enhances nitric oxide bioactivity in aortas of spontaneously hypertensive rats

机译：芝麻素增强自发性高血压大鼠主动脉中一氧化氮的生物活性

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The blood pressure lowering effect of sesamin has been demonstrated to be associated with the increase in vascular nitric oxide (NO) biological activity by our previous studies and others. The present study was designed to explore the underlying mechanisms involved in the effect of sesamin on aortic NO bioactivity in spontaneously hypertensive rats (SHRs). Sesamin was orally administered for 8 consecutive weeks in SHRs. Systolic blood pressure (SBP) was measured using the tail-cuff method. The aortas were isolated and in vitro vascular reactivity studies were performed. Superoxide anion production in carotid arteries was assessed by dihydroethidium fluorescence staining. The protein expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (P-eNOS), dihydrofolate reductase (DHFR), nicotinamide adenine dinucleotide phosphate oxidase subunit p47phox, and copper, zinc superoxide dismutase (Cu/Zn-SOD) in aortas was detected by Western blotting. The dimeric form of eNOS in aortas was determined by low-temperature sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Aortic level of nitrotyrosine and activities of antioxidant enzymes, namely, total SOD (T-SOD), glutathione peroxidase (GPx) and catalase were also detected. In SHRs, sesamin treatment reduced SBP, improved vascular relaxation induced by acetylcholine and enhanced aortic NO bioactivity. Sesamin treatment enhanced NO biosynthesis in SHR aortas was due to upregulated P-eNOS and suppressed eNOS uncoupling, and the latter effect might be attributed to decreased nitrotyrosine and upregulated DHFR. Sesamin also reduced the NO oxidative inactivation and decreased the superoxide anion production through downregulation of p47phox and amelioration of eNOS uncoupling. In addition, sesamin treatment did not alter the levels of GPx and catalase activity but obviously reduced the compensatory elevated T-SOD activity and Cu/Zn-SOD protein expression. Chronic treatment with sesamin could reduce hypertension and improve endothelial dysfunction through enhancement of NO bioactivity in SHR aortas.
机译：我们先前的研究和其他研究已证明，芝麻素的降压作用与血管一氧化氮（NO）生物活性的增加有关。本研究旨在探讨芝麻素对自发性高血压大鼠（SHRs）主动脉NO生物活性影响的潜在机制。芝麻素在SHR中连续8周口服。使用尾袖套法测量收缩压（SBP）。分离主动脉并进行体外血管反应性研究。通过二氢乙啶荧光染色评估颈动脉中超氧阴离子的产生。血管内皮一氧化氮合酶（eNOS），磷酸化eNOS（P-eNOS），二氢叶酸还原酶（DHFR），烟酰胺腺嘌呤二核苷酸磷酸氧化酶亚基p47phox以及主动脉中铜，锌超氧化物歧化酶（Cu / Zn-SOD）的蛋白质表达为通过蛋白质印迹检测。通过低温十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）确定主动脉中eNOS的二聚体形式。还检测到主动脉的硝基酪氨酸水平和抗氧化酶的活性，即总SOD（T-SOD），谷胱甘肽过氧化物酶（GPx）和过氧化氢酶。在SHR中，芝麻素治疗可降低SBP，改善乙酰胆碱引起的血管舒张并增强主动脉NO的生物活性。芝麻素处理增强了SHR主动脉中NO的生物合成，这是由于P-eNOS上调和eNOS解偶联受到抑制，后者的作用可能归因于硝基酪氨酸减少和DHFR上调。芝麻素还通过下调p47phox和改善eNOS解偶联来减少NO的氧化失活并减少超氧阴离子的产生。此外，芝麻素处理并没有改变GPx和过氧化氢酶的活性，但明显降低了补偿性T-SOD活性和Cu / Zn-SOD蛋白表达的升高。芝麻素的慢性治疗可通过增强SHR主动脉中的NO生物活性来降低高血压并改善内皮功能障碍。

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