The protective effects of vitamin E on lung injury caused by high temperature and PM in COPD rats.
10.12047/j.cjap.5788.2019.061
- Author:
Jiang-Tao LIU
1
;
Bin LUO
1
;
Xiao-Tao HE
1
;
Lan-Yu LI
1
;
Sheng-Gang XU
2
Author Information
1. Institute of Occupational Health and Environmental Health, School of Public Health, Lanzhou University, Lanzhou
2. Medical College of Hexi University, Zhangye 734000, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Chemokine CCL2;
metabolism;
Hot Temperature;
adverse effects;
Lung;
physiopathology;
Male;
Nitric Oxide Synthase Type II;
metabolism;
Particulate Matter;
adverse effects;
Pulmonary Disease, Chronic Obstructive;
drug therapy;
Random Allocation;
Rats;
Rats, Wistar;
Tumor Necrosis Factor-alpha;
metabolism;
Vitamin E;
pharmacology
- From:
Chinese Journal of Applied Physiology
2019;35(4):293-296
- CountryChina
- Language:Chinese
-
Abstract:
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 PM.
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 PM (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 PM could inhibit the lung function of COPD rats significantly (P＜0.05); the level of MCP-1 was increased significantly in PM-exposure groups (P＜0.05); iNOS was increased significantly in the groups of high temperature (P＜0.05). Compared with the single-PM 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 PM could aggravate the inflammation of COPD rats. As an antioxidant, vitamin E may protect the lung from the damage effects.
