In vivo evaluation of purified methanolic extract and medicagenic acid saponin from Chenopodium bonus-henricus L. roots in a rotenone-induced Parkinson’s disease model

A purified methanolic extract (PME) and compound S [3-O-β-glucuronopyranosyl-medicagenic acid-28-β-xylopyranosyl(1→4)-α-rhamnopyranosyl(1→2)-α-arabinopyranosyl ester], isolated from the roots of Chenopodium bonus-henricus L., were investigated in vivo using a rotenone-induced model of Parkinson’s disease. Biochemical parameters, including malondialdehyde (MDA) levels and reduced glutathione (GSH) content, were measured in brain homogenates of treated mice. Rotenone administration alone induced significant neurotoxicity, evidenced by a 50% reduction in GSH levels and a 150% increase in MDA levels compared with the control group (untreated animals). Co-administration with PME preserved GSH levels by 50% and decreased MDA production by 52%, while compound S preserved GSH levels by 60% and reduced MDA levels by 48% compared with animals treated with pure rotenone. Additionally, preservation of brain histoarchitecture was observed in groups co-treated with rotenone and either the purified MeOH extract or compound S. These results demonstrate that both PME and compound S exert statistically significant neuroprotective effects against rotenone-induced neurotoxicity. This protective activity is likely attributable to their antioxidant properties, including the mitigation of oxidative stress and the neutralization of free radicals. Overall, the findings highlight the critical role of oxidative stress in rotenone-induced toxicity and support the potential of antioxidant-based therapies for Parkinson’s disease.