Abstract
Background: 1-Nitropyrene (1-NP), an environmental pollutant derived from nitro-polycyclic aromatic hydrocarbons, poses serious environmental hazards. Vernonia amygdalina (VA), commonly known as bitter leaf, is widely used in folk medicine due to its pharmacological properties.
Objectives: This study investigated the pharmacological role of VA in 1-NP-induced hepatopulmonary oxido-inflammatory stress responses in a murine model.
Methods: Experimental animals were randomly divided into five groups of seven rats each and orally treated with 1-NP (250 mg/kg) alone or in combination with VA (50 mg/kg and 100 mg/kg) for 7 consecutive days. Then, glutathione, reactive oxygen and nitrogen species, nitric oxide (NO), and lipid peroxidation levels were biochemically assessed alongside the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase-4 (GPX4), glutathione-S-transferase (GST), and myeloperoxidase (MPO). Eventually, the enzyme-linked immunosorbent assay was utilized to evaluate regulated upon activation, normal T cell expressed and secreted (RANTES), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β).
Results: VA administration markedly ameliorated 1-NP-induced oxido-inflammatory hepatopulmonary damage by upregulating enzymatic and non-enzymatic antioxidants while diminishing proinflammatory proteins as observed by the reduced levels of RANTES, TNF-α, IL-1β, NO, and MPO activities.
Conclusion: Overall, VA prevented 1-NP-induced hepatopulmonary damage by enhancing antioxidant enzymes and inhibiting proinflammatory markers, thereby protecting the organs.