Lim Hye-Sun, Kim Joong-Sun, Moon Byeong Cheol, Ryu Seung Mok, Lee Jun, Park Gunhyuk
Herbal Medicine Resources Research Center, Korea Institute of Oriental Medicine, 111 Geonjae-ro, Naju-si 58245, Korea.
Antioxidants (Basel). 2019 Nov 21;8(12):574. doi: 10.3390/antiox8120574.
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.
氧化应激在帕金森病(PD)中多巴胺能神经元的退化过程中起着重要作用。神经元中氧化还原稳态的改变会干扰多种生物学过程,最终导致神经元死亡。氧化损伤已被确认为PD进展的主要机制之一。多项研究强调了超氧自由基在诱导神经元毒性方面的关键作用。僵蚕,即被白僵菌(Bals.)Vuill.感染的家蚕幼虫干燥体,因其多种药理作用而被用于传统医学。在本研究中,僵蚕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作用。在PD小鼠模型中,僵蚕治疗改善了行为障碍,保护了多巴胺能神经元,并维持了多巴胺水平。在此,我们研究了僵蚕对MPTP诱导的小鼠PD的保护作用,并探讨了其潜在的作用机制,重点关注氧化信号传导。在MPTP诱导的PD中,僵蚕促进了运动障碍的恢复,防止了多巴胺耗竭,并保护黑质致密部(SNpc)或纹状体(ST)中的多巴胺能神经元免于退化。此外,僵蚕上调了抗氧化反应介质,如超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽(GSH)、血红素加氧酶1(HO-1)和烟酰胺腺嘌呤二核苷酸磷酸(NAD(P)H)脱氢酶(NQO1)。因此,僵蚕治疗减轻了氧化应激,改善了行为障碍,并保护免受MPTP诱导毒性中的多巴胺耗竭。