芝麻素对自发性高血压大鼠的降压作用及机制

Anti-hypertensive effect and mechanism of sesamin in spontaneously hypertensive rats

目的:观察芝麻素(Ses)对自发性高血压大鼠(SHR)的降压作用,并探讨其可能机制。方法:SHR 35只,随机分为SHR模型组、Ses160、80、40 mg/(kg·d)、卡托普利(Cap)30 mg/(kg·d),另设WKY正常对照组,于给药16周后,颈总动脉插管测收缩压(SBP)、舒张压(DBP)及平均血压(MBP),Griess Reagent法测主动脉中一氧化氮(NO)含量,化学比色法测主动脉中过氧化氢(H2O2)含量,RT-PCR观察主动脉内皮型一氧化氮合酶(eNOS)、p22phox及p47phoxmRNA表达。结果:与SHR组相比,Ses160、80 mg/kg组SBP、DBP、MAP均显著降低(P<0.01,P<0.05),主动脉中NO含量显著提高(P<0.01),eNOS mRNA表达显著增加(P<0.01,P<0.05),p22phox、p47phoxmRNA表达显著减少(P<0.01,P<0.05)。Ses各剂量组H2O2含量显著降低(P<0.01)。结论:芝麻素通过上调SHR主动脉中eNOS mRNA的表达,使内皮细胞合成和释放NO增多;下调主动脉NADPH氧化酶p22phox和p47phoxmRNA的表达,使NO活性恢复,发挥降血压的作用。

Objective：To observe the anti-hypertensive effects of sesamin （ Ses） and its potential mechanism in the spontaneously hypertensive rats （SHR）.Methods：Thirty-five SHRs were randomized into groups of SHR model,administration of sesamin in dose of 160,80 and 40 mg/（kg＆#183; d） as well as captopril（Cap）in dose of 30 mg/（kg＆#183; d）.Another 7 Wistar-Kyoto （WKY） rats were added as negative controls.All rats were undergone measurement of the systolic blood pressure（ SBP） ,diastolic blood pressure（ DBP） and mean blood pressure（ MBP） via inserting a cannula into the carotids,and deter-mination of the aortic nitric oxide （NO） and hydrogen peroxide （H2O2） levels with Griess reagent.Reverse transcription polymerase chain reaction（RT-PCR） was performed to determine the expression of aortic eNOS,p22phox and p47phox mRNA.Results：The SBP,DBP and MAP were significantly decreased in groups treated with sesamin in dose of 160 and 80 mg/kg（P＆lt;0.01,P＆lt;0.05）,whereas the aortic NO level was markedly elevated （P＆lt;0.01） and eNOS mRNA expression was remarkably up-regulated（P＆lt;0.01,P＆lt;0.05）,and p22phox and p47phox mRNA were significantly down-regulated（P＆lt;0.01, P＆lt;0.05）,as compared with those in the SHR group.In addition,aortic H2O2 levels were reduced in groups treated with diverse dose of sesamin（P＆lt;0.01）.Conclusion：Sesamin may function in anti-hypertension for SHR through up-regulating the level of eNOS mRNA to facilitate increased synthesis and release of NO in the endothelial cells,while down-regulating the subunits of p22phox and p47phox mRNA expression in aortas to enhance the NO activity.