Therapeutic potential of 2S-hesperidin against the hepatotoxic effects of dichlorvos in rats.

Abstract

Dichlorvos (DDVP) is an organophosphate insecticide that enhances food production and repels disease vectors. However, it provokes cytotoxicity. 2S-hesperidin (2S-HES) is a potent antioxidant, anti-inflammatory, and anti-lipidemic flavanone. Regardless, the 2S-HES impact on DDVP-occupied hepatic injury remains fuzzy. We evaluated the therapeutic potential of 2S-HES in a rat model of DDVP-elicited hepatic intoxication. Forty-two rats were randomly allotted to seven groups (n = 6/condition): control, DDVP (8 mg kg⁻¹day⁻¹), DDVP with 2S-HES (50 and 100 mg kg⁻¹day⁻¹), DDVP with atropine, and 2S-HES alone (50 and 100 mg kg⁻¹day⁻¹). DDVP was administered orally for 7 days, followed by 14 days of 2S-HES chemotherapy. 2S-HES intervention partially mitigated DDVP-triggered alterations in leakage enzymes (ALT, AST, ALP, LDH-5), total protein, albumin, globulin, bilirubin, electrolytes, ion-transporters, lipid profiles, and HMG-CoA reductase. Furthermore, 2S-HES partially reversed DDVP-provoked increases in hepatic H₂O₂, NO, and malondialdehyde; transposed DDVP-mediated decreased liver GSH amount and activities of GST, SOD, catalase, and GPx; attenuated DDVP-triggered upregulated NF-κB-p65 and caspase-3; and abated DDVP-engendered repressed interleukin-10 mRNA expression. Cytoarchitectural analyses authenticated the 2-HES reduction in DDVP-evoked hepatocellular vacuolation. Altogether, 2S-HES elicited promising alternative or adjunctive therapy for partially mitigating DDVP-incited hepatic injury by attenuating leakage enzymes, ionoregulatory disruptions, ion pump inhibition, dyslipidemias, oxidative stress, inflammation, and apoptosis.