Table 3.
Disease | Components | Effects, materials and methods | Mechanism | References |
---|---|---|---|---|
| ||||
HD | Extract | Improve systemic 3-NP-induced behavioral impairment and extended survival in rat | No effect on the inhibition of succinate dehydrogenase activity; (↓) 3-NP-induced intracellular Ca2+ elevations and cytotoxicity of striatal neurons | 73 |
Rb1, Rb5 Rc | (↓) Glutamate-induced apoptosis in YAC128 medium spiny neurons | (↓) Glutamate-induced Ca2+ responses in cultured MSN | 74 | |
ALS | Rb2 | (↑) Transcriptional activation of the Cu, Znsuperoxide dismutase gene | (↑) Induction of the SOD1 gene; (↑) specific binding of the AP2 transcription factor | 89 |
MS | Polysaccharides | (↓) Encephalitogenic response during EAE | (↓) The proliferation of autoreactive T cells and the production of IFN-γ, IL-1β and IL-17; (↑) the generation of immunosuppressive regulatory T cells (Tregs) through the activation of transcription factor, Foxp3 | 97 |
ALS, amyotrophic lateral sclerosis; AP2, activating protein 2; EAE, experimental autoimmune encephalomyelitis; HD, Huntington’s disease; IFN- γ, interferon-gamma; IL, interleukin; MS, multiple sclerosis; MSN, medium spiny striatal neuronal cultures; SOD1, superoxide dismutase 1; 3-NP, 3-nitropropionic acid.