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-1β 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.
Highlights
Parkinson’s disease (PD), the second most common agerelated neurodegenerative disease after Alzheimer’s disease, is affecting approximately 1% of the population over 60 years of age
We found that mice in MPTP group showed a remarkable decline in total distance of movement, total entries relative to those of the control group in Y-maze test (Figures 1(c)–1(e))
MPTP mice with Bushen-Yizhi Formula (BSYZ) in both high dose and middle dose could alleviate this decrease. These results confirmed that BSYZ administration could alleviate MPTP-induced motor impairment
Summary
Parkinson’s disease (PD), the second most common agerelated neurodegenerative disease after Alzheimer’s disease, is affecting approximately 1% of the population over 60 years of age. PD is characterized with motor symptoms such as akinesia, bradykinesia, rigidity, tremor, and the progressive loss of dopaminergic neurons in the substantia nigra and axonal terminals in the striatum [1,2,3]. PD is reported to be caused by mitochondrial dysfunction, oxidative stress, and chronic inflammation, but its underlying mechanisms are still unknown [4,5,6]. Increasing reports showed neuroinflammation plays a dominant role in the pathogenesis of PD [6, 7]. It is well known that the activated microglial cells, the major source of proinflammatory factors and cytokines, are closely related to the dopaminergic neurons loss and survival in PD [4, 8].
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