Curcumin alleviates cigarette smoke–induced inflammatory and pulmonotoxic responses via modulation of inflammo-oxidoregulation and angiogenesis-related pathways in male Wistar rats
摘要
Cigarette smoke (CS) remains the major environmental factor responsible for the occurrence and progression of chronic obstructive pulmonary disease (COPD), with oxidative damage and systemic inflammation playing major roles. Curcumin, a dietary polyphenol, is widely acclaimed for its potent antioxidant and anti-inflammatory properties. This study was designed to assess the possible effects of curcumin on oxidative damage and inflammatory responses associated with CS exposure in the lungs of rats. Thirty (30) male albino rats (180–220 g) were exposed to normal air or cigarette smoke (whole-body exposure) for 90 min/day for six (6) weeks. They were then divided into six groups (n = 5) and treated for 2 weeks, as follows: Control, CS + vehicle, CS + curcumin [10 mg/kg body weight (b.w.)], CS + curcumin (20 mg/kg b.w.), curcumin (10 mg/kg b.w.), and curcumin (20 mg/kg b.w.). Bronchoalveolar lavage fluid (BALF) was collected, and lung tissues were excised after the sacrifice. Exposed groups exhibited significant increase (p < 0.05) in inflammatory indices and, immune cell infiltration into the BALF. There was a significant increase (p < 0.05) in the oxidative damage markers measured by H2O2, nitric oxide, malondialdehyde, myeloperoxidase activity. Antioxidant enzymes: superoxide dismutase, catalase, and glutathione peroxidase and reduced glutathione level, were significantly impaired in the lungs of CS-exposed rats. Furthermore, CS exposure invoked increased alpha-antitrypsin, vascular endothelial growth factor, and tumour necrosis factor — alpha and depleted IL–10 expressions. These biochemical alterations resulted in severe histological impairment of the lung tissues. Nevertheless, curcumin dose-dependently alleviates CS-induced systemic aberrations. Thus, our findings suggest that curcumin might provide some remedies against CS-induced lung injuries in rodent models.