School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang 453003, Henan, China; Clinical Medical Center of Tissue Engineering and Regeneration, Xinxiang Medical University, Xinxiang 453003, Henan, China.
School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang 453003, Henan, China.
Brain Res Bull. 2023 Oct 1;202:110762. doi: 10.1016/j.brainresbull.2023.110762. Epub 2023 Sep 12.
Parkinson's disease (PD) is the second largest neurodegenerative disorder caused by the decreased number of dopaminergic (DAc) neurons in the substantia nigra pars compacta (SNpc). There is evidence that oxidative stress can contribute degeneration of DAc neurons in SNpc which is mainly caused by apoptotic cell death. Thus, suppressing oxidative stress and apoptosis of DAc neurons is an effective strategy to mitigate the progress of PD. Astaxanthin (AST) is a carotenoid, which mainly exists in marine organisms and is a powerful biological antioxidant. In this study, we aimed to determine the neuroprotective effect of AST on paraquat (PQ) -induced models of PD in vitro and in vivo. Here, we showed that AST significantly enhanced cell survival of SH-SY5Y cells against PQ toxicity by suppressing apoptotic cell death and oxidative stress. Moreover, we found that AST significantly ameliorated PQ-induced behavioral disorders associated with PD in C57BL/6 J mice and the damage to DAc neurons in the SNpc of mice. Lastly, we found that the neuroprotective effects of AST were conducted through inhibiting PQ-induced activation of MAPK signaling. In conclusion, our study indicates that AST had a strong protective effect on PQ-induced oxidative stress and antagonized apoptotic cell death in SH-SY5Y cells and PQ-induced mice PD model, which might provide new insights of AST for PD treatment.
帕金森病（PD）是由黑质致密部（SNpc）中多巴胺能（DAc）神经元数量减少引起的第二大神经退行性疾病。有证据表明，氧化应激可导致 SNpc 中的 DAc 神经元退化，主要是由细胞凋亡引起的。因此，抑制 DAc 神经元的氧化应激和凋亡是减轻 PD 进展的有效策略。虾青素（AST）是一种类胡萝卜素，主要存在于海洋生物中，是一种强大的生物抗氧化剂。在这项研究中，我们旨在确定 AST 对体外和体内百草枯（PQ）诱导的 PD 模型的神经保护作用。在这里，我们表明 AST 通过抑制细胞凋亡和氧化应激显著增强了 SH-SY5Y 细胞对 PQ 毒性的存活能力。此外，我们发现 AST 显著改善了 C57BL/6J 小鼠 PQ 诱导的与 PD 相关的行为障碍和小鼠 SNpc 中 DAc 神经元的损伤。最后，我们发现 AST 的神经保护作用是通过抑制 PQ 诱导的 MAPK 信号通路的激活来实现的。总之，我们的研究表明，AST 对 PQ 诱导的氧化应激和拮抗 SH-SY5Y 细胞和 PQ 诱导的小鼠 PD 模型中的细胞凋亡具有很强的保护作用，这可能为 PD 的治疗提供了新的思路。
