Diosgenin Attenuates Lipopolysaccharide-Induced Parkinson’s Disease by Inhibiting the TLR/NF-κB Pathway
| Autor: | Danhong Chen, Shuyan Wu, Bingyu Li, Qian Li, Zhijian Huang, Pengli Xu, Zhixian Jiang |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Lipopolysaccharides
Male 0301 basic medicine Lipopolysaccharide Nitric Oxide Synthase Type II Substantia nigra Diosgenin Pharmacology medicine.disease_cause Proinflammatory cytokine Antiparkinson Agents Rats Sprague-Dawley Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Forelimb medicine Animals Cells Cultured Cell Line Transformed Tyrosine hydroxylase Superoxide Dismutase General Neuroscience NF-kappa B Brain Parkinson Disease General Medicine Toll-Like Receptor 2 Rats Disease Models Animal Psychiatry and Mental health Clinical Psychology TLR2 030104 developmental biology chemistry TLR4 Geriatrics and Gerontology Reactive Oxygen Species Neuroglia 030217 neurology & neurosurgery Oxidative stress Signal Transduction |
| Zdroj: | Journal of Alzheimer's Disease. 64:943-955 |
| ISSN: | 1875-8908 1387-2877 |
| Popis: | Background Parkinson's disease (PD) is a neurodegenerative disease characterized by loss of dopaminergic neurons in the substantia nigra. Diosgenin is a natural steroid saponin which was shown to play a beneficial role in Alzheimer's disease. Objective This study sought to investigate the potential effect of diosgenin on a rat model of PD. Methods Sprague Dawley rats were subjected to intra-striatal injection of lipopolysaccharide (LPS) and treated with diosgenin. Stepping, Whisker, and Cylinder tests were carried out to determine the motor function, and the expression of tyrosine hydroxylase was detected by immunohistochemistry. The levels of multiple proinflammatory cytokines, oxidative stress related factors and proteins involved in Toll-like receptor (TLR)/nuclear factor kappa B (NF-κB) pathway were measured. The synergistic effect of environment enrichment on diosgenin was also investigated. Results Intra-striatal injection of LPS caused motor deficits in rats, induced inflammatory response and oxidative stress response, and activated the TLR/NF-κB pathway both in vivo and in vitro. Diosgenin could attenuate the LPS-induced alterations. Enriched environment enhanced the effect of diosgenin to ameliorate the LPS-induced motor deficits in rats and decreased the protein levels of TLR2, TLR4, and nuclear NF-κB in diosgenin treated PD rats. Conclusion Diosgenin had a beneficial effect in LPS-induced rat PD models, by suppressing the TLR/NF-κB signaling pathway. Environmental enrichment could play a synergistic effect with diosgenin, by enhancing the inhibitory effect of diosgenin on the TLR/ NF-κB signaling pathway. |
| Databáze: | OpenAIRE |
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