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Batryticatus Bombyx Protects Dopaminergic Neurons against MPTP-Induced Neurotoxicity by Inhibiting Oxidative Damage

机译:Batryticatus Bombyx通过抑制氧化损伤来保护多巴胺能神经元免受MPTP诱导的神经毒性

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摘要

Oxidative stress plays an important role in the degeneration of dopaminergic neurons in Parkinson’s disease (PD). Altered redox homeostasis in neurons interferes with several biological processes, ultimately leading to neuronal death. Oxidative damage has been identified as one of the principal mechanisms underlying the progression of PD. Several studies highlight the key role of superoxide radicals in inducing neuronal toxicity. Batryticatus Bombyx (BB), the dried larva of L. infected by (Bals.) Vuill., has been used in traditional medicine for its various pharmacological effects. In the present study, BB showed a beneficial effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity by directly targeting dopaminergic neurons. Treatment with BB improved behavioral impairments, protected dopaminergic neurons, and maintained dopamine levels in PD mouse models. Here, we investigated the protective effects of BB on MPTP-induced PD in mice and explored the underlying mechanisms of action, focusing on oxidative signaling. In MPTP-induced PD, BB promoted recovery from impaired movement, prevented dopamine depletion, and protected against dopaminergic neuronal degradation in the substantia nigra pars compacta (SNpc) or the striatum (ST). Moreover, BB upregulated mediators of antioxidative response such as superoxidase dismutase (SOD), catalase (CAT), glutathione (GSH), Heme oxygenase 1 (HO-1), and NAD(P)H (nicotinamide adenine dinucleotide phosphate) dehydrogenase (NQO1). Thus, treatment with BB reduced the oxidative stress, improved behavioral impairments, and protected against dopamine depletion in MPTP-induced toxicity.
机译:氧化应激在帕金森氏病(PD)中的多巴胺能神经元变性中起重要作用。神经元中氧化还原稳态的改变会干扰几种生物学过程,最终导致神经元死亡。氧化损伤已被确定为PD病情发展的主要机制之一。多项研究强调了超氧自由基在诱导神经元毒性中的关键作用。 Batryticatus Bombyx(BB)是受(Bal。)Vuill。感染的L.的干燥幼虫,由于其各种药理作用已被用于传统医学。在本研究中,BB通过直接靶向多巴胺能神经元对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的神经毒性显示出有益的作用。用BB治疗可以改善行为障碍,保护多巴胺能神经元,并在PD小鼠模型中保持多巴胺水平。在这里,我们调查了BB对MPTP诱导的小鼠PD的保护作用,并探讨了潜在的作用机制,重点是氧化信号传导。在MPTP诱导的PD中,BB促进了运动障碍的恢复,防止了多巴胺的消耗,并保护了黑质致密部(SNpc)或纹状体(ST)的多巴胺能神经元降解。此外,BB上调了抗氧化反应的介体,例如超氧化物酶歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽(GSH),血红素加氧酶1(HO-1)和NAD(P)H(烟酰胺腺嘌呤二核苷酸磷酸)脱氢酶(NQO1) )。因此,用BB进行治疗可减少氧化应激,改善行为障碍,并防止MPTP诱导的毒性中的多巴胺消耗。

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