Silibinin extenuates arsenic instigated oxidative pulmonary damage and fibrosis in rats

Abstract

Arsenic (As) and its compounds were widely used as a medicine in the past years for the treatment of such diseases as diabetes, psoriasis, syphilis, skin ulcers and joint diseases. Long-term exposure to arsenic from drinking-water and food can cause cancer and skin lesions. It has also been associated with cardiovascular, lung diseases and diabetes. Its exposure could cause severe oxidative stress and fibrotic injuries in lung tissue. Due to the antioxidant and anti-inflammatory properties of siibinin (SB), the present study investigated its effects on As-induced pulmonary toxicity. For the experimental study, twenty four male rats were randomly categorized into four groups of six. Initially, the first and fourth groups were treated intragastrically with normal saline and SB (80 mg/kg) for 28 consecutive days, respectively. The second and third groups were treated with As (5mg/kg BW) and As along with SB (80 mg/kg BW) for 28 consecutive days, respectively, At the end of the experimental tenure, the animals were anesthetized with ketamine and xylazine, and lung tissue samples were collected for biochemical and histological examinations. The results showed that As significantly increased hydroxyproline (HP) and lipid peroxidation (LPO) and decreased the lung tissue antioxidant capacity. In addition, myeloperoxidase (MPO) activity increased significantly, while glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) activity declined substantially. The administration of therapeutic doses of SB could prevent the oxidative, fibrotic, and inflammatory effects of As-induced lung toxicity, and these changes were consistent with histological observations. In conclusion, SB may improve the antioxidantdefense of lung tissue and prevent the spread of inflammation and the development of As-induced fibrotic injuries by enhancing antioxidant enzymes and preventing inflammatory cell infiltration.