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首页> 外文期刊>Neurochemical Research >Neuroprotective Effects of Withania somnifera Dunal.: A Possible Mechanism
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Neuroprotective Effects of Withania somnifera Dunal.: A Possible Mechanism

机译:Withania somnifera Dunal的神经保护作用:可能的机制

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摘要

Present study was carried out to understand the possible mechanism of neuroprotective action of the root extract of Withania somnifera Dunal (WS). The study is focused on WS mediated inhibition of nitric oxide production, which is known to mediate neurodegeneration during stress. Adult mice (28 ± 5 g) were exposed to restraint stress for 30 days. Activity of NADPH diaphorase (NADPH-d) and factors (Acetylcholine, serotonin and corticosterone), which regulates NADPH-d activity were studied. Treatment with WS extract for 30 days during stress, significantly reversed the stress induced NADPH-d activation. Observations suggest that inhibition of NADPH-d by WS is not a direct effect of extract on NADPH-d, instead it inhibits via suppressing corticosterone release and activating cholineacetyltransferase, which in turn increase serotonin level in hippocampus to inhibit NADPH-d. Together, the main mechanism underlying the neuroprotective effects of WS can be attributed to its role in the down regulation of nNOS and neurochemical alterations of specific neurotransmitter systems. These observations thus suggest that WS root extract could be developed as a potential preventive or therapeutic drug for stress induced neurological disorders.
机译:进行本研究以了解Withania somnifera Dunal(WS)根提取物的神经保护作用的可能机制。这项研究的重点是WS介导的一氧化氮产生抑制作用,已知该作用可在压力下介导神经变性。成年小鼠(28±5 g)受到束缚压力30天。研究了NADPH心肌黄递酶(NADPH-d)的活性以及调节NADPH-d活性的因子(乙酰胆碱,5-羟色胺和皮质酮)。在压力下用WS提取物处理30天,可显着逆转压力诱导的NADPH-d活化。观察结果表明,WS对NADPH-d的抑制作用不是提取物对NADPH-d的直接作用,而是通过抑制皮质酮释放和激活胆碱乙酰基转移酶来抑制NADPH-d,这反过来会增加海马中的血清素水平,从而抑制NADPH-d。在一起,WS的神经保护作用的主要机制可以归因于它在nNOS的下调和特定神经递质系统的神经化学改变中的作用。因此,这些观察结果表明,WS根提取物可以开发成用于应激诱导的神经系统疾病的潜在预防或治疗药物。

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