内源性硫化氢在帕金森病中的作用研究进展

Research Progress on the Role of Endogenous Hydrogen Sulfide in Parkinson’s Disease

摘要: 帕金森病(Parkinson’s disease, PD)是仅次于阿尔茨海默病的第二大神经退行性疾病，以中脑黑质致密部中的多巴胺能神经元变性丢失和残存神经元胞质中形成嗜酸性路易小体为主要病理特征，临床多表现为静止性震颤、运动迟缓和肌肉僵直。PD的发病机制十分复杂，至今尚未完全阐明。但现有证据表明炎症反应、氧化应激和细胞凋亡与PD密切相关。硫化氢(H2S)是继一氧化氮(NO)和一氧化碳(CO)之后的第三种内源性气体信号分子，具有抗神经系统炎症、氧化应激和细胞凋亡的作用。近年来研究发现，内源性H2S可通过p38-丝裂原活化蛋白激酶/核转录因子Kappa B、Kelch样环氧氯丙烷相关蛋白1-核因子E2相关因子2/抗氧化反应元件、蛋白激酶C/磷脂酰肌醇3-激酶/蛋白激酶B/糖原合成激酶-3β等相关信号通路，分别发挥抗炎、抗氧化应激和抗凋亡的作用。本文阐述了内源性H2S相关信号通路在PD中的研究进展，旨在为临床治疗PD提供理论依据。

Abstract: Parkinson’s disease (PD) is the second largest neurodegenerative disease after Alzheimer’s disease. Its main pathological features are the degeneration and loss of dopaminergic neurons in the dense part of substantia nigra and the formation of eosinophilic lewy bodies in the cytoplasm of residual neurons. Its clinical manifestations are static tremor, bradykinesia and muscle stiffness. The path-ogenesis of PD is extremely complex and has not been absolutely clarified so far, but the existing evidence shows that inflammatory response, oxidative stress and apoptosis are closely related to PD. H2S is the third endogenous gas signal molecule after NO and CO, which has the effects of anti-oxidant stress, nervous system inflammation and apoptosis. In recent years, it has been found that endogenous H2S can pass p38-mitogen-activated protein kinase/nuclear factor kappa-B, Kelch-like ECH-associated protein-1-NF-E2-related factor 2/Anti-oxidant reaction element, protein kinase C/phosphatidylinositol 3-kinase/protein kinase B/glycogen synthase kinase-3β and other related signal pathways, which play the roles of anti-inflammatory, anti-oxidative stress and anti-apoptosis respectively. This review describes the research progress of endogenous H2S-related signaling pathways in PD, aims at providing a theoretical basis for the clinical treatment of PD.