褪黑素可防止ng -硝基- l -精氨酸甲酯高血压大鼠左心室纤维化,但不能防止左心室肥厚。

Ludovit Paulis, Olga Pechanova, Josef Zicha, Kristina Krajcirovicova, Andrej Barta, Vaclav Pelouch, Michaela Adamcova, Fedor Simko
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引用次数: 39

摘要

目的:褪黑素具有降低血压、提高一氧化氮利用率和清除自由基的作用。然而,关于褪黑素对与血流动力学负荷相关的病理性左心室重构的影响,缺乏数据。设计:我们研究褪黑素是否能够预防与N(G)-硝基- l -精氨酸甲酯(L-NAME)诱导的高血压相关的左心室肥厚(LVH)和纤维化。方法:将雄性Wistar大鼠分为4组:对照组、L-NAME (50 mg/kg / d)、褪黑素(10 mg/kg / d)和L-NAME加褪黑素。每周无创测量血压。处理5周后处死大鼠,测定左心室一氧化氮合酶(NOS)活性、内皮细胞和诱导细胞一氧化氮合酶表达、胶原蛋白、羟脯氨酸和共轭二烯水平。结果:L-NAME可抑制NOS活性,增加偶联二烯浓度,升高血压,诱导LVH和纤维化(胶原蛋白和羟脯氨酸水平升高)。在L-NAME治疗中加入褪黑素不能阻止NOS活性的减弱和LVH的发展,仅部分预防高血压。然而,褪黑素的施用完全阻止了共轭二烯浓度的增加和左心室纤维化的发展。各组间NOS表达无明显差异。结论:褪黑素对l - name诱导的高血压大鼠左室纤维化的发生及氧化负荷的增加具有抑制作用。褪黑素的抗纤维化作用似乎独立于其对NOS活性的影响,可能与其抗氧化特性有关。
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Melatonin prevents fibrosis but not hypertrophy development in the left ventricle of NG-nitro-L-arginine-methyl ester hypertensive rats.

Objective: Melatonin was shown to reduce blood pressure, enhance nitric oxide availability and scavenge free radicals. There is, however, a shortage of data with respect to the effect of melatonin on pathological left ventricular remodelling associated with haemodynamic overload.

Design: We investigated whether melatonin was able to prevent left ventricular hypertrophy (LVH) and fibrosis associated with N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension.

Methods: Four groups of male Wistar rats were investigated: control, L-NAME (50 mg/kg per day), melatonin (10 mg/kg per day) and L-NAME plus melatonin. Blood pressure was measured non-invasively each week. After 5 weeks of treatment the animals were killed and nitric oxide synthase (NOS) activity, endothelial and inducible NOS expression, the level of collagenous proteins, hydroxyproline and conjugated dienes in the left ventricle were determined.

Results: The administration of L-NAME inhibited NOS activity, increased conjugated dienes concentration, elevated blood pressure and induced LVH and fibrosis (indicated by increased collagenous proteins and hydroxyproline levels). The addition of melatonin to L-NAME treatment failed to prevent the attenuation of NOS activity and the development of LVH and prevented hypertension only partly. The administration of melatonin, however, completely prevented the increase in conjugated dienes concentration and the development of left ventricular fibrosis. NOS expression was not different among experimental groups.

Conclusion: Melatonin prevented the development of left ventricular fibrosis and the increase in oxidative load in rats with L-NAME-induced hypertension. The antifibrotic effect of melatonin seems to be independent of its effects on NOS activity and might be linked to its antioxidant properties.

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