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补肾益智方通过抑制帕金森病小鼠模型中的NLRP3炎性小体激活减轻神经炎症

Bushen-Yizhi Formula Alleviates Neuroinflammation via Inhibiting NLRP3 Inflammasome Activation in a Mouse Model of Parkinson's Disease.

作者信息

Mo Yousheng, Xu Erjin, Wei Renrong, Le Baoluu, Song Lei, Li Dongli, Chen Yonggen, Ji Xiaotian, Fang Shuhuan, Shen Jiangang, Yang Cong, Wang Qi

机构信息

Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 12 Airport Road, Baiyun District, Guangzhou 510405, China.

Faculty of Traditional Medicine, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam.

出版信息

Evid Based Complement Alternat Med. 2018 Aug 26;2018:3571604. doi: 10.1155/2018/3571604. eCollection 2018.

Abstract

Parkinson's disease (PD), the second most common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although the molecular mechanisms underlying dopaminergic neuronal degeneration in PD remain unclear, neuroinflammation is considered as the vital mediator in the pathogenesis and progression of PD. Bushen-Yizhi Formula (BSYZ), a traditional Chinese medicine, has been demonstrated to exert antineuroinflammation in our previous studies. However, it remains unclear whether BSYZ is effective for PD. Here, we sought to assess the neuroprotective effects and explore the underlying mechanisms of BSYZ in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine- (MPTP-) induced mouse model of PD. Our results indicate that BSYZ significantly alleviates the motor impairments and dopaminergic neuron degeneration of MPTP-treated mice. Furthermore, BSYZ remarkably attenuates microglia activation, inhibits NLPR3 activation, and decreases the levels of inflammatory cytokines in MPTP-induced mouse brain. Also, BSYZ inhibits NLRP3 activation and interleukin-1 production of the 1-methyl-4-phenyl-pyridinium (MPP) stimulated BV-2 microglia cells. Taken together, our results indicate that BSYZ alleviates MPTP-induced neuroinflammation probably via inhibiting NLRP3 inflammasome activation in microglia. Collectively, BSYZ may be a potential therapeutic agent for PD and the related neurodegeneration diseases.

摘要

帕金森病(PD)是第二常见的神经退行性疾病,其特征是黑质中多巴胺能神经元逐渐丧失。尽管PD中多巴胺能神经元变性的分子机制尚不清楚,但神经炎症被认为是PD发病机制和进展中的重要介质。补肾益智方(BSYZ)是一种中药,在我们之前的研究中已被证明具有抗神经炎症作用。然而,BSYZ对PD是否有效仍不清楚。在此,我们试图在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的PD小鼠模型中评估BSYZ的神经保护作用并探索其潜在机制。我们的结果表明,BSYZ可显著减轻MPTP处理小鼠的运动障碍和多巴胺能神经元变性。此外,BSYZ可显著减轻小胶质细胞活化,抑制NLPR3活化,并降低MPTP诱导的小鼠脑中炎性细胞因子的水平。此外,BSYZ可抑制1-甲基-4-苯基吡啶离子(MPP)刺激的BV-2小胶质细胞的NLRP3活化和白细胞介素-1产生。综上所述,我们的结果表明,BSYZ可能通过抑制小胶质细胞中NLRP3炎性小体的活化来减轻MPTP诱导的神经炎症。总体而言,BSYZ可能是治疗PD及相关神经退行性疾病的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca4/6129340/5a6a1bb1df51/ECAM2018-3571604.001.jpg

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