The effect of captopril on lipopolysaccharide-induced lung inflammation

ABSTRACT

Purpose: As an angiotensin converting enzyme (ACE) inhibitor, the effects of captopril on inflammation has been previously examined. Captopril has been shown to have anti-inflammatory and antioxidant effects. Imbalance in the oxidant/antioxidant system is one of the major causes of inflammation. In the present study, the effects of captopril on total and differential white blood cells (WBC), oxidative stress andlung histopathological changes produced by lipopolysaccharide (LPS) were investigated in rat. Materials and Method: The rats were divided into: control (saline-treated), LPS (1 mg/kg), 12.5, 25 or 50 mg/kg captopril-treated before LPS administration (LPS+Cap12.5, LPS+Cap25 and LPS+Cap50) and Cap-treated, 50 mg/kg before saline administration (as positive control group)groups. The levels of total and percentage of differential WBC in blood, and the oxidative stress index in the serum were evaluated. Lung histopathological changes were also examined. Results: In the LPS group, total WBC count, percentage of neutrophils, basophils, eosinophils, and monocytes in the blood, oxidative stress indices in serum, lung pathological changes were significantly higher than the control group (p < 0.05 to p < 0.001). Pathological changes of lung, serum oxidative stress indices of LPS+Cap50 group, total WBC counts of LPS+Cap25 and LPS+Cap50 groups, as well as percentage of neutrophils, monocytes, and basophils in LPS+Cap50 group and percentage of eosinophils in LPS+Cap50 and LPS+Cap25 groups, were significantly decreased compared to the LPS group (p < 0.05 to p < 0.001). Conclusion: The results of this study showed that captopril dose-dependently reduced total and differential WBC counts, while it improved serum oxidant/antioxidant biomarkers and histopathological changes in LPS-treated rats. These results indicate a therapeutic potential for captopril on systemic inflammation and oxidative stress against LPS-induced lung injuries.

KEYWORDS:

• captopril
• inflammation
• lipopolysaccharide
• lung
• oxidative stress

Acknowledgment

This study was financially supported by a grant from the Research Council of Mashhad University of Medical Sciences. The results of this article are a part of the Pharm D thesis of Javad Boskabadi.

Disclosure of potential conflicts of Interest

No potential conflicts of interest were disclosed.