Research Progress on the Antagonism of Aluminum-Induced Neurotoxicity by Ginsenosides

Abstract

Aluminum (Al) was a nonessential toxic metal in the environment. Al exposure had been widely demonstrated to cause cognitive impairment and neuronal damage. However, the neurotoxicology mechanism of Al was still not summarized through the oxidative stress, inflammation, apoptosis, and gut microbiota. Ginsenosides, natural active components derived from ginseng, had garnered significant attention due to its antioxidant and neuroprotective properties. Although the neurotoxic mechanisms of Al had been elucidated, the treatment of ginsenosides on Al exposure was elusive. This review explores the suppressive feasibility of ginsenosides on the Al-induced neurotoxicity through oxidative stress, inflammatory factors, apoptosis, and intestinal microbiota. Ginsenoside Rb1, Rk3, and Rg1 exhibits anti-inflammatory, anti-oxidative stress, anti-apoptosis, and refinement the gut microbiota composition. But the direct evidence is scarce in the Al-induce neuro disease. Compared with donepezil, ginsenosides exhibit a synergistic advantage encompassing pathological intervention—neuroprotection—metal clearance. Thus, ginsenosides may have potential therapeutic intervention to mitigate Al-induced neurotoxicity. However, the precise mechanisms underlying these effects warrant further investigation.