Background: Nanoparticle's formulation of natural products is recently posed effective medicinal applications against different clinical disorders. Zearalenone (ZEA) is certainly considered one among mycotoxins which might be from corn, sorghum and wheat. In the liver, ZEA is metabolized into α- and β-zearalenol, which are considered more toxic than ZEA. The present study investigated biochemical and histological ameliorative effects of Melittin (MEL) and MEL-loaded chitosan nanoparticles (Cs-NPs), a primary polypeptide in the venom of honeybee (Apis mellifera) against hepatotoxicity induced by ZEA. The ionic gelation process was used to make MEL-loaded chitosan-TPP nanoparticles that contained chitosan, MEL, and TPP salt. Rats were divided into 4 groups. Control: given orally 2.7 mg/kg b.w. of 1% DMSO saline, T1: given orally 2.7 mg/kg b.w. of ZEA, T2: given orally 2.7 mg/kg b.w. of ZEA, then given orally MEL 40 µg/kg b.w after intoxication. T3: given orally 2.7 mg/kg b.w. of ZEA, then given orally MEL loaded on Cs-NPs 40 µg/kg b.w after intoxication. DMSO saline and ZEA were given to rats twice a week for two weeks, while MEL/MEL nanoparticles were given three-time weekly for one month after ZEA intoxication, Serum ALT, AST, ALP, Albumin, Total protein, alpha-fetoprotein, TNF-α, and total antioxidant status was assessed. Histological changes in the rat's liver were matched with biochemical changes.

Results: FT-IR indicated that MEL was successfully loaded into CS-NPs. TEM with average diameter of 37.5 nm and a spherical shape for MEL-loaded chitosan-TPP nanoparticles. The encapsulation efficiency (EE%) of MEL in chitosan-TPP nanoparticles was 82.35%. our study demonstrated that MEL-loaded chitosan-TPP nanoparticles confer ameliorative effects against ZEA-induced hepatic biochemical and histological alteration.

Conclusion: The present study demonstrated that nanoparticles like chitosan-tripolyphosphate (TPP) can increase the antihepatotoxic properties of MEL and can be utilized as a potent agent in the treatment of chemical-induced hepatotoxicity.