AI Article Synopsis
- - The study investigates the protective effects of purified panaxadiol saponin (PDSF) and purified panaxatriol saponin (PTSF) against Parkinson’s disease (PD) in rat models, specifically focusing on motor dysfunction and damage to brain cells caused by rotenone exposure.
- - Results show that PDSF provides significant protection to crucial brain cells, maintains the integrity of the blood-brain barrier, and helps regulate inflammatory factors, while PTSF fails to offer similar protection and may even worsen conditions when combined with PDSF.
- - The findings suggest that PDSF has strong potential for both prevention and treatment of PD due to its ability to inhibit neuroinflammation and protect against cell
Article Abstract
Background: The effects of individual panaxadiol saponin and panaxatriol saponin on rodent models of Parkinson's disease (PD) have been recognized. However, it is not clear whether purified total ginsenosides as an entirety has effect against PD in rat model. This study compared the protective effects of a purified panaxadiol saponin fraction (PDSF), a purified panaxatriol saponin fraction (PTSF), and their mixtures against the rotenone (ROT)-induced PD in rats.
Methods: Potential effects of PDSF, PTSF, and their mixtures against motor dysfunction and impairments of nigrostriatal dopaminergic neurons (DN), blood-brain barrier (BBB), cerebrovascular endothelial cells (CEC), and glial cells were measured in the models of ROT-induced PD rats and cell damage. Pro-inflammatory NF-kB p65 (p65) activation was localized in DN and other cells in the striatum.
Results: PDSF and PTSF had a dose-dependent effect against motor dysfunction with a larger effective dose range for PDSF. PDSF protected CEC, glial cells, and DN in models of PD rats and cell damage, while PTSF had no such protections. Chronic ROT exposure potently activated p65 in CEC with enhanced pro-inflammatory and decreased anti-inflammatory factors and impaired BBB in the striatum, PDSF almost completely blocked the ROT-induced p65 activation and maintained both anti- and pro-inflammatory factors at normal levels and BBB integrity, but PTSF aggravated the p65 activation with impaired BBB. Furthermore, PTSF nullified all the effects of PDSF when they were co-administrated.
Conclusion: PDSF had significant protective effect against the ROT-induced PD in rats by protecting CEC, glial cells, and DN, likely through inhibiting NF-κB p65 in CEC from triggering neuroinflammation, and also directly protecting glial cells and neurons against ROT-induced toxicity. PDSF has great potential for preventing and treating PD.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385176 | PMC |
| http://dx.doi.org/10.1016/j.jgr.2024.05.002 | DOI Listing |
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