Objective: To investigate the effects of vitamin E on the respiratory function impairment in rats with chronic obstructive pulmonary disease (COPD) after exposed to high temperature and PM2.5.
Methods: Fifty-four 7-week-old SPF male Wistar rats were randomly divided into 9 experimental groups (n=6). The rat COPD model was established by lipopolysaccharide (LPS) and smoke exposure. After modeled, the rats were tracheal instilled with PM2.5 (0 mg/ml, 3.2 mg/ml) and intraperitoneally injected with vitamin E at the dose of 40 mg/kg (20 mg/ml). Part of rats (high temperature groups) were then exposed to high temperature (40℃), once (8 h) a day for three consecutive days. After the last exposure, the lung function of rats was detected. The expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) were detected by corresponding ELISA kits.
Results: Compared with the control group, exposure of high temperature and PM2.5 could inhibit the lung function of COPD rats significantly (P＜0.05); the level of MCP-1 was increased significantly in PM2.5-exposure groups (P＜0.05); iNOS was increased significantly in the groups of high temperature (P＜0.05). Compared with the single-PM2.5 exposure groups, TNF-α in lung was decreased in the normal temperature health group and high temperature COPD group (P＜0.05) after treated with vitamin E; MCP-1 was decreased in all vitamin E-treated groups (P＜0.05); the decreased iNOS only appeared in the group of high temperature with vitamin E treatment.
Conclusion: High temperature and PM2.5 could aggravate the inflammation of COPD rats. As an antioxidant, vitamin E may protect the lung from the damage effects.