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首页> 外文期刊>Neurochemical research >Neuroprotective efficacy of eugenol and isoeugenol in acrylamide-induced neuropathy in rats: behavioral and biochemical evidence.
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Neuroprotective efficacy of eugenol and isoeugenol in acrylamide-induced neuropathy in rats: behavioral and biochemical evidence.

机译:丁子香酚和异丁香酚在丙烯酰胺诱导的大鼠神经病变中的神经保护作用:行为和生化证据。

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The primary objective of this investigation was to assess the neuroprotective efficacy of spice active principles namely Eugenol (Eug) and isoeugenol (IE) in an acrylamide (ACR) neuropathy model in rats. In the present study, ACR administration (50 mg/kg bw, i.p. 3 times/week) for 5 weeks to growing rats caused typical symptoms of neuropathy. We found that treatment of ACR rats with spice active principles (10 mg/kg bw, for 5 weeks) caused marked improvement in gait score and responses in a battery of behavioral tests. Terminally, both spice active principles markedly attenuated ACR-induced markers of oxidative stress viz., reactive oxygen species (ROS), malondialdehyde (MDA) and nitric oxide (NO) in sciatic nerve (SN) as well as brain regions (cortex Ct, cerebellum Cb). Treatment with Eug restored the reduced glutathione levels in SN and brain regions. Interestingly, both spice active principles effectively diminished ACR-induced elevation in cytosolic calcium levels and acetylcholinesterase activity in SN and Ct. Further, the diminished activity of ATPase among ACR rats was enhanced in SN and restored in brain regions. Furthermore, Eug treatment significantly offset ACR-induced depletion in dopamine levels in brain regions. Collectively our findings suggest the propensity of these spice active principles to attenuate ACR-induced neuropathy. Further studies are necessary to understand the precise molecular mechanism/s by which these spice active principles attenuate neuropathy. Nevertheless, our data clearly demonstrate the beneficial effects of spice active principles in ACR-induced neuropathy in rats and suggest their possible therapeutic usage as an adjuvant in the management of other forms of neuropathy in humans.
机译:这项研究的主要目的是评估在丙烯酰胺(ACR)神经病模型中香料活性成分即丁香酚(Eug)和异丁香酚(IE)的神经保护作用。在本研究中,向生长中的大鼠施用ACR(50 mg / kg体重,腹腔内注射,每周3次,每周5次)引起神经病的典型症状。我们发现,用香料有效成分(10 mg / kg体重,持续5周)治疗ACR大鼠,在一系列行为测试中,步态得分和反应明显改善。最终,两种香料活性成分均显着减弱了ACR诱导的坐骨神经(SN)以及大脑区域(大脑皮层Ct,大脑中的活性氧,活性氧(ROS),丙二醛(MDA)和一氧化氮(NO))的标记。小脑Cb)。用Eug进行治疗可恢复SN和大脑区域降低的谷胱甘肽水平。有趣的是,两种香料活性成分均有效地降低了ACR诱导的SN和Ct胞质钙水平升高以及乙酰胆碱酯酶活性。此外,SN中增强了ACR大鼠中ATPase活性的降低,并在大脑区域中得以恢复。此外,Eug治疗可显着抵消ACR诱导的大脑区域多巴胺水平的消耗。总的来说,我们的发现表明这些香料活性成分倾向于减弱ACR引起的神经病。有必要进行进一步的研究以了解这些香料活性成分减弱神经病的确切分子机制。然而,我们的数据清楚地证明了香料活性成分对大鼠ACR引起的神经病变的有益作用,并暗示了它们可能作为治疗人类其他形式神经病变的佐剂的治疗用途。

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