ALLICIN AMELIORATES PARAQUAT-INDUCED PULMONARY INJURY IN RATS

Background: Paraquat (PQ) is a highly toxic herbicide that induces severe multi-organ injury through excessive oxidative stress, inflammation, and apoptosis, particularly affecting the lung and liver. Allicin, the principal bioactive organosulfur compound of garlic, possesses potent antioxidants and anti-inflammatory properties; however, its protective role against PQ-induced pulmonary injury remains poorly understood. Objective: This study investigated the protective effects of allicin against PQ-induced lung injury, with particular emphasis on the Nrf2/HO-1 and NF-κB/NLRP3 signaling pathways. Methods: Male Sprague–Dawley rats were randomly allocated into four groups: control, PQ, allicin 20 mg/kg + PQ, and allicin 50 mg/kg + PQ. Allicin was administered orally for seven consecutive days before a single intraperitoneal injection of PQ (30 mg/kg). Twenty-four hours later, oxidative stress indices, inflammatory mediators, and apoptosis-related markers were evaluated using biochemical assays, ELISA, histopathology, and immunohistochemistry. Results: PQ administration caused marked pulmonary injury, evidenced by elevated tissue MDA, IL-1β, NF-κB, TNF-α, NLRP3, and caspase-3, while significantly decreasing GSH, SOD, Nrf2, HO-1, and Bcl-2. Histopathological examination confirmed severe structural damage in the lung. Allicin pretreatment dose-dependently ameliorated biochemical and histopathological alterations, restored antioxidant defenses, activated the Nrf2/HO-1 pathway, suppressed NF-κB/NLRP3-mediated inflammation, reduced apoptotic signaling, and markedly improved pulmonary architecture. Conclusion: Allicin confers significant protection against PQ- induced lung injury, likely through coordinated enhancement of antioxidant defenses and attenuation of inflammatory and apoptotic pathways. These findings support allicin as a promising candidate for further investigation against PQ-induced lung toxicity.