1. Inhibitory Effects of Astragaloside IV on Bleomycin-Induced Pulmonary Fibrosis in Rats Via Attenuation of Oxidative Stress and Inflammation
- Author
-
Hua Yang, Wei-Na Yu, and Li-Feng Sun
- Subjects
0301 basic medicine ,Pathology ,medicine.medical_specialty ,Pulmonary Fibrosis ,Immunology ,Pharmacology ,Bleomycin ,medicine.disease_cause ,Superoxide dismutase ,Rats, Sprague-Dawley ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Pulmonary fibrosis ,medicine ,Immunology and Allergy ,Animals ,chemistry.chemical_classification ,Inflammation ,Reactive oxygen species ,Lung ,medicine.diagnostic_test ,biology ,Dose-Response Relationship, Drug ,business.industry ,Saponins ,Malondialdehyde ,medicine.disease ,Triterpenes ,Rats ,Oxidative Stress ,030104 developmental biology ,Bronchoalveolar lavage ,medicine.anatomical_structure ,chemistry ,030220 oncology & carcinogenesis ,biology.protein ,business ,Oxidative stress - Abstract
In this study, we investigated the effects of astragaloside IV (As-IV) on pulmonary fibrosis and its mechanisms of action. Sprague-Dawley rats were used in a model of pulmonary fibrosis induced by an intratracheal instillation of bleomycin (BLM). Rats were intraperitoneally injected with As-IV (10, 20, 50 mg/kg) daily for 28 days, while the rats in control and BLM groups were injected with a saline solution. The effects of As-IV treatment on pulmonary injury were evaluated with the lung wet/dry weight ratios, cell counts, and histopathologic. Oxidative stress was evaluated by detecting the levels of malondialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and reactive oxygen species (ROS) in lung tissue. Inflammation was assessed by measuring the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in bronchoalveolar lavage fluid (BALF). The results indicated that As-IV treatment remarkably ameliorated BLM-induced pulmonary fibrosis and attenuated BLM-induced oxidative stress and inflammation. Our findings indicate that As-IV-mediated suppression of fibroproliferation may contribute to the anti-fibrotic effect against BLM-induced pulmonary fibrosis. Its mechanisms of action are associated with inhibiting oxidative stress and inflammatory response. In summary, our study suggests a therapeutic potential of As-IV in the treatment of pulmonary fibrosis.
- Published
- 2016