Astragalus polysaccharide protects against neuron degeneration and mitochondrial dysfunction in Parkinson's disease by upregulating CEND1.

Abstract

BACKGROUND: possesses antioxidant, anti-inflammatory, and neuroprotective properties. APS was previously revealed to exert neuroprotective effects in experimental PD models. However, the underlying mechanism remains poorly understood. Therefore, our study was designed to reveal the molecular mechanism through which APS exerts neuroprotective effects in PD. METHODS: -knockout (CEND1-KO) mice were used to confirm whether APS exhibits the neuroprotective effects via a CEND1-dependent mechanism. Behavior tests, immunohistochemical staining, and western blotting were performed to examine mouse motor dysfunction, neuronal injury, and mitochondrial dysfunction. RESULTS: . APS administration successfully improved motor deficits, neuronal injury, and mitochondrial impairments in WT (wild-type) mice, but failed to protect against PD in CEND1-KO mice. CONCLUSION: APS exerts its neuroprotective effects in PD by preventing mitochondrial dysfunction through increasing CEND1 expression.