Quercetin-3-O-β-D-Glucopyranoside-Rich Fraction from Spondias mombin Leaves Halted Responses from Oxidative Stress, Neuroinflammation, Apoptosis, and Lipid Peroxidation in the Brain of Dichlorvos-Treated Wistar Rats

HIGHLIGHTS: Protective efficacy of Quercetin-3-O-β-D-glucopyranoside-rich fraction (Q3G-RF) from Spondias mombin role on Dichlorvos (DDVP) toxicity was studied. DDVP induced cognitive and locomotive impairment, free radicals, oxidative stress, neuroinflammation, and apoptosis in the brain of rats. Q3G-RF from S. mombin leaves prevented DDVP-induced cognitive and locomotion impairment in the rats. Q3G-RF from S. mombin leaves prevented DDVP-induced deficits in fluid intake and body weight of the rats. Q3G-RF from S. mombin leaves abated DDVP-induced inhibition of AChE, BuChE in the brain sections of rats. Q3G-RF from S. mombin leaves reversed elevated activities APEH, DPP-IV and POP in the brain sections of rats exposed to DDVP. Q3G-RF from S. mombin leaves revoked the DDVP-induced oxidative stress in the brain sections of rats. Q3G-RF from S. mombin leaves prevented DDVP-induced neuroinflammation in the brain sections of rats. Q3G-RF from S. mombin leaves reversed DDVP-induced apoptosis in the brain sections of rats. Q3G-RF from S. mombin leaves assuaged DDVP neural toxicity in the brain sections of rats via anti-oxidative and anti-inflammatory mechanisms. ABSTARCT: The study investigated the prophylactic efficacy of Quercetin-3-O-β-D-glucopyranoside-rich fraction (Q3G-RF) from Spondias mombin leaves on oxidative and neuronal damages in the brain sections of dichlorvos (DDVP)-treated female Wistar rats. Female Wistar rats assigned into 5 groups of 12 rats each were orally treated with appropriate regimens. Group 1 received sunflower oil. Group 2 received DDVP (8.8 mg/kg). Group 3 received Q3G-RF (100 mg/kg). Group 4 received DDVP + Q3G-RF (50 mg/kg). Group 5 received DDVP + Q3G-RF (100 mg/kg). Q3G-RF reversed DDVP-induced cognitive deficits in the rats and reversed rearing activity impairment; it protected against the following DDVP-induced activities: inhibition of cholinesterases (acetylcholinestere (AChE), butyrylcholinesterase (BuChE)), elevated marker-enzymes (acylpeptide hydrolase (APEH), dipeptidylpeptidase IV (DPP-IV), prolyl oligopeptidase (POP)), oxidative stress (total thiol, malondialdehyde, hydrogen peroxide (H(2)O(2)), reduced glutathione and the activities glutathione S-transferase, catalase, superoxide dismutase, and glutathione peroxidase), inflammation (myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), nitric oxide, interleukin-1 beta (IL-1β)), and apoptosis (caspase-3) in the hippocampus, striatum, and prefrontal cortex of the experimental rats exposed to DDVP (p < 0.05). Conclusively, the neuroprotective effects of Q3G-RF on DDVP-induced toxicity in the hippocampus, striatum, and prefrontal cortex in brain of rats suggests its potent antioxidant, prophylactic, and chemotherapeutic properties.