Abstract:
Air particulate matters (PM), with diesel exhaust particles (DEP) as a typical component, have been reported in many studies to be responsible for the toxic effects of air pollution. Curcumin, a phenolic compound in turmeric, has been established to possess potent anti-inflammatory, antioxidant, anticarcinogenic and antimutagenic properties. This research aims to determine the effects of Curcumin on DEP-induced toxicity in the kidney and liver of male albino rats. Rats were exposed to either 30 μg/kg or 60 μg/kg mDEP by nasal instillation and other groups were pre-treated with 20 mg/kg of curcumin intraperitoneally before mDEP exposure. Serum biomarkers, oxidative stress and inflammatory biomarkers were all assayed in the tissues. The results showed that mDEP caused significant (P<0.0001) elevation in serum Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Bilirubin and N-acetyl-cystein-(NAC)-activated creatinkinase (CK-NAC) activities, increased Malonaldehyde (MDA) and conjugated deienes (CDs) but decreased Glutathione (GSH) levels. All these effects were reversed by curcumin. There were significant inductions in Glutathione peroxidase (GPx), Catalase, Superoxide dismutase and Glutathione reductase activities on exposure to diesel exhaust particles and curcumin was able to ameliorate these effects. There were significant inductions in the pro-inflammatory: Interleukin-8, Tumor Necrotic Factor-α (TNF- α), Nuclear Factor Kappa B (NF-ĸB), and Kidney injury molecule-1 (KIM-1) genes but reduction in Interleukin-10 mRNA expressions. Also, there were inductions in Aryl hydrocarbon receptor (Ahr), Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT), Nuclear factor-erythroid factor 2-related factor 2 (Nrf2), and Heme oxygenase (HO-1) mRNA expression in the presence of mDEP. These effects were ameliorated by curcumin. In summary, the present study shows that curcumin has the ability to protect against DEP-induced nephron-hepatotoxicity in a mechanism that may involve Nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and Nuclear Factor Kappa B (NF-ĸB) mediated pathways.
