| First Author | Kim C | Year | 2015 |
| Journal | J Neuroinflammation | Volume | 12 |
| Pages | 236 | PubMed ID | 26683203 |
| Mgi Jnum | J:298195 | Mgi Id | MGI:6477427 |
| Doi | 10.1186/s12974-015-0455-9 | Citation | Kim C, et al. (2015) Hypoestoxide reduces neuroinflammation and alpha-synuclein accumulation in a mouse model of Parkinson's disease. J Neuroinflammation 12:236 |
| abstractText | BACKGROUND: Deposition of alpha-synuclein and neuroinflammation are key pathological features of Parkinson's disease (PD). There is no cure for the disease; however, targeting the pathological features might be available to modulate the disease onset and progression. Hypoestoxide (HE) has been demonstrated as a NF-kappaB modulator, thereby acting as a potential anti-inflammatory and anti-cancer drug. METHODS: In order to assess the effect of HE in a mouse model of PD, mThy1-alpha-syn transgenic mice received intraperitoneal (IP) injections of either vehicle or HE (5 mg/kg) daily for 4 weeks. RESULTS: Treatment of HE decreased microgliosis, astrogliosis, and pro-inflammatory cytokine gene expression in alpha-syn transgenic mice. HE administration also prevented the loss of dopaminergic neurons and ameliorated motor behavioral deficits in the alpha-syn transgenic mice, and alpha-synuclein pathology was significantly reduced by treatment of HE. In addition, increased levels of nuclear phosphorylated NF-kappaB in the frontal cortex of alpha-syn transgenic mice were significantly reduced by HE administration. CONCLUSIONS: These results support the therapeutic potential of HE for PD and other alpha-synuclein-related diseases. |
