鱼油联合假马齿苋对3-硝基丙酸氧化应激大鼠的神经保护作用

Denny Joseph Manual Kollareth, M. Muralidhara
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摘要

目的:尽管有证据表明n-3多不饱和脂肪酸(n-3 PUFA)对神经退行性疾病有有益作用,但由于PUFA可能会增加氧化应激,导致脂质过氧化物的形成,因此提出了一些担忧。因此,建议添加抗氧化剂/植物化学物质。本研究将鱼油与假马齿苋(Bacopa monnieri, BM)联合使用,采用慢性3-硝基丙酸(NPA)大鼠神经毒性模型,研究鱼油+假马齿苋(Bacopa monnieri, BM)的神经保护倾向。材料与方法:雄性生长大鼠给药NPA (10 mg/kg bw, 14d)后,分别添加FO (2 mL/kg bw)、BM (100 mg/kg bw)或FO+BM组合(FO+BM),持续14d。结果:FO+BM大鼠对NPA诱导的行为改变具有较高的保护程度。此外,NPA管理导致脑区(纹状体- St,小脑- Cb)氧化标志物显著升高,而在补充FO+BM的大鼠中有明显的保护作用。在所有补充组中,St中的GSH水平都恢复了。这种组合还使大脑区域的抗氧化酶活性显著正常化。此外,仅在FO+BM大鼠中,St中显著减少的多巴胺水平部分恢复。然而,该组合对NPA诱导的线粒体功能障碍没有保护作用。结论:目前的数据清楚地表明,鱼油与植物化学物质(如BM)联合使用有可能增强神经保护程度,从而为氧化应激介导的神经退行性疾病的治疗/管理提供了一种改进的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroprotective Efficacy of A Combination of Fish Oil and Bacopa Monnieri Against 3-Nitropropionic Acid Induced Oxidative Stress in Rats
AIM: Despite the evidence on the beneficial effects of n-3 polyunsaturated fatty acids (n-3 PUFA) on neurodegenerative conditions, several concerns have been raised since PUFA may increase oxidative stress resulting in the formation of lipid peroxides. Hence addition of antioxidants/phytochemicals is recommended. In the present study, we have used fish oil (FO) in combination with Bacopa monnieri (BM) and examined the neuroprotective propensity of the combination (FO+BM) employing chronic 3-nitropropionic acid (NPA) model of neurotoxicity in rats. MATERIALS AND METHODS: Growing male rats administered NPA (10 mg/kg bw, 14d) were supplemented with FO (2 mL/kg bw), BM (100 mg/kg bw) or combination (FO+BM) for 14 days. RESULTS: Higher degree of protection was discernible among FO+BM rats against NPA induced behavioral alterations. Further, NPA administration resulted in significantly elevated oxidative markers in brain regions (striatum- St, cerebellum- Cb) while robust protection was evident among rats supplemented with FO+BM. Depleted GSH levels in St were restored among all the supplemented groups. The combination also predominantly normalized the activity of antioxidant enzymes in brain regions. Further, significantly depleted dopamine levels in St were partially restored only among FO+BM rats. However, the combination did not offer protection against NPA induced mitochondrial dysfunction. CONCLUSION: The present data clearly suggests that it is possible to enhance the degree of neuroprotection by a combination of FO with phytochemicals (such as BM) and thus provides an improved strategy for the treatment/ management of oxidative stress mediated neurodegenerative conditions.
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