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Hesperidin-Loaded Chitosan Nanoparticles Restore Hepatic Homeostasis by Targeting Nrf2/HO-1 and NF-κB/p53 Signaling
Ekramy M Elmorsy1, Ayat B Al-Ghafari2,3, Huda A Al Doghaither2
1Center for Health Research, Northern Border University, Arar, Saudi Arabia.
Environmental Toxicology
|March 21, 2026
Summary
Hesperidin chitosan nanoparticles (HES-CNPs) offer superior protection against Malathion-induced liver damage in rats compared to hesperidin alone. HES-CNPs activate antioxidant pathways and inhibit inflammation and apoptosis, demonstrating significant hepatoprotective effects.
Area of Science:
- Pharmacology and Toxicology
- Nanotechnology in Medicine
- Hepatology
Background:
- Malathion (MAL) is an organophosphate insecticide known to induce significant liver toxicity.
- Oxidative stress, inflammation, and apoptosis are key mechanisms underlying MAL-induced hepatotoxicity.
- Hesperidin (HES), a flavonoid, possesses antioxidant and anti-inflammatory properties, but its efficacy can be limited by bioavailability.
Purpose of the Study:
- To evaluate the hepatoprotective efficacy of hesperidin encapsulated in chitosan nanoparticles (HES-CNPs) against Malathion-induced liver injury in a rat model.
- To compare the protective effects of HES-CNPs with free hesperidin (HES).
- To elucidate the molecular mechanisms underlying the hepatoprotective action of HES-CNPs.
Main Methods:
- Ninety male Wistar rats were divided into control, HES, HES-CNPs, MAL, MAL+HES, and MAL+HES-CNPs groups.
- Hepatotoxicity was induced by Malathion (27 mg/kg BW) administration for four weeks.
- HES and HES-CNPs were administered at 100 mg/kg BW.
- Biochemical markers (liver enzymes, total protein, bilirubin, lipids), oxidative stress markers (antioxidant enzymes, MDA, ROS, GSH), molecular markers (apoptotic and inflammatory genes, Nrf2, Bcl-2), and DNA damage (8-OHdG) were assessed.
- Histopathological and ultrastructural examinations of liver tissue were performed.
- In silico studies were conducted to assess HES binding affinity to target proteins.
Main Results:
- Malathion exposure significantly impaired liver function, induced oxidative stress, elevated proapoptotic and inflammatory markers, and caused DNA damage.
- HES-CNPs treatment demonstrated significantly greater hepatoprotection than HES alone (p < 0.05).
- HES-CNPs normalized liver biomarkers, restored antioxidant status, reduced lipid peroxidation, suppressed inflammation and apoptosis, enhanced Nrf2 and Bcl-2 expression, and attenuated DNA damage.
- Histopathological and ultrastructural analyses confirmed improved liver integrity with HES-CNPs treatment.
- In silico analysis revealed HES binding to proteins involved in oxidative stress, apoptosis, and inflammation.
Conclusions:
- Hesperidin-loaded chitosan nanoparticles (HES-CNPs) exhibit superior hepatoprotective effects against Malathion-induced liver toxicity compared to free hesperidin.
- The protective mechanism involves the activation of the Nrf2/HO-1 antioxidant pathway and the inhibition of NF-κB/p53-mediated inflammation and apoptosis.
- HES-CNPs represent a promising nanocarrier system for enhancing the therapeutic potential of hesperidin in treating liver damage.
