Abstract
Backgrounds and aims: Cigarette smoke (CS) is known to cause airway inflammation. Cryptotanshinone(CTS), a major ingredients of tanshinones, has been reported to have anti-inflammatory, antioxidative and other therapeutical effects. We designed this study to investigate the potential protective effects of CTS on CS-induced airway inflammation and oxidative stress in mice and the possible mechanisms.
Methods: BALB/c mice were exposed to CS for 2.5 h twice daily, 6 days per week for 4 weeks. Low-dose (15 mg/kg·d) or high-dose (30 mg/kg·d) CTS were administered intraperitoneally 1 h before CS exposure. Bronchoalveolar lavage fluid (BALF) was acquired for detection of pro-inflammatory cytokine levels. Lung tissue was collected for histological examination, superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels, and western blot assays for lectin-like oxidized low-density lipoprotein-1 receptor (LOX-1) and phosphorylated NF-κB p65.
Results: CTS administration attenuated CS-induced thickening of the airway epithelium and peribronchial inflammatory cell infiltration. Moreover, CTS remarkably reduced the CS-induced elevation of TNF-α (12.99±3.37 vs 23.08±2.17 pg/ml), IL-17 (40.04±16.51 vs 124.84±7.04 pg/ml), and MCP-1 (33.85±7.76 vs 79.06±11.98 pg/ml) levels in BALF (all p<0.05). CTS pretreatment also prevented CS-induced elevation in MDA levels and decrease in SOD activities (p<0.05). Furthermore, the CS-induced expression of LOX-1 and the phosphorylation of p65 were also attenuated by CTS.
Conclusions: These results suggest that CTS attenuated inflammation and oxidative stress induced by CS. The LOX-1 and NF-κB pathway may involve in this process.
- Copyright ©the authors 2016
