首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Molecular Mechanisms of Nigella sativa - and Nigella sativa Exercise-Induced Cardiac Hypertrophy in Rats
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Molecular Mechanisms of Nigella sativa - and Nigella sativa Exercise-Induced Cardiac Hypertrophy in Rats

机译:大鼠Nigella sativa的分子机制 - 大鼠中的Nigella sativa运动诱导的心脏肥厚

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Background . In our lab, we demonstrated cardiac hypertrophy induced by long-term administration of Nigella sativa (Ns) with enhanced function. Therefore, we aim to investigate the molecular mechanisms of Ns-induced cardiac hypertrophy, compare it with that induced by exercise training, and explore any possible synergistic effect of these two interventions. Method . Twenty adult Wistar male rats were divided into control (C), Ns-fed (N.s.), exercise-trained (Ex.), Ns-fed exercise-trained (N.s.Ex.) groups. 800?mg/kg of Ns was administered orally to N.s. rats. Ex. rats were trained on a treadmill with speed 18?m/min and grade 32° for two hours daily, and the N.s.Ex. group underwent both interventions. After 8 weeks, Immunohistochemical slides of the left ventricles were prepared using rat growth hormone (GH), insulin-like growth factor I (IGF-I), angiotensin-II receptors 1 (AT-I), endothelin-I (ET-1), Akt-1, and Erk-1. Cell diameter and number of nuclei were measured. Results . Cardiomyocyte diameter, number of nuclei, GH, and Akt were significantly higher in N.s, Ex., and N.s.Ex groups compared with the controls. IGF-I, AT-1, and ET-1 were significantly higher in Ex. rats only compared with the controls. Erk-1 was lower in N.s., Ex., and N.s.Ex. compared with the controls. Conclusion . We can conclude that Ns-induced cardiac hypertrophy is mediated by the GH-IGF I-PI3P-Akt pathway. Supplementation of Ns to exercise training protocol can block the upregulation of AT-I and ET-1. The combined N.s. exercise-induced cardiac hypertrophy might be a superior model of physiological cardiac hypertrophy and be used as a prophylactic therapy for athletes who are engaged in vigorous exercise activity.
机译:背景 。在我们的实验室中,我们展示了通过增强功能的Nigella Sativa(NS)的长期施用的心脏肥厚。因此,我们的目的是研究NS诱导的心脏肥大的分子机制,将其与运动培训引起的诱导,并探讨这两个干预措施的任何可能的协同效应。方法 。二十个成年Wistar雄性大鼠分为对照(c),Ns-Fed(N.S.),运动培训(例如),NS-Fed运动培训(N.S.EX.)组。 800?mg / kg ns口服给n.s.老鼠。前任。每天2小时,速度18°/ min训练大鼠在速度18?m / min和32°等级,以及N.S.EX.群体接受过两次干预措施。 8周后,使用大鼠生长激素(GH),胰岛素样生长因子I(IGF-1),血管紧张素-II受体1(AT-I),内皮素-1(ET-1(ET-1)制备左心室的免疫组织化学载玻片。 ),AKT-1和ERK-1。测量细胞直径和核数。结果 。与对照相比,N.S,EX的心肌细胞直径,核,GH和Akt的数量显着高。 IGF-I,AT-1和ET-1在前面显着高。大鼠只与对照相比。 ERK-1在N.S.,EX。和N.S.EX.中较低。与对照相比。结论 。我们可以得出结论,NS诱导的心脏肥厚由GH-IGF I-PI3P-AKT途径介导。 NS对行使培训协议的补充可以阻止AT-I和ET-1的上调。合并的N.S.运动诱导的心脏肥大可能是生理心脏肥大的优异模型,用作从事剧烈运动活动的运动员的预防性疗法。

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