Key result
Captopril dose-dependently reduced total and differential WBC counts, improved serum oxidative stress indices, and reduced lung histopathological changes in LPS-treated rats (p<0.05 to p<0.001).
Why the study?
Does captopril reduce inflammation and oxidative stress in rats with LPS-induced lung injury?
Does captopril reduce inflammation and oxidative stress in rats with LPS-induced lung injury?
p-value: p=< 0.05 to < 0.001
Captopril demonstrates dose-dependent anti-inflammatory and antioxidant effects in a rat model of LPS-induced lung injury, suggesting potential therapeutic benefits for systemic inflammation.
Hypothesis-generating for captopril in inflammatory lung injury; leaves open clinical translation and requires human trials.
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.
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Boskabadi et al. (2018) studied lipopolysaccharide-induced lung inflammation. captopril vs. LPS alone and saline control was evaluated on total and differential white blood cells (WBC), oxidative stress and lung histopathological changes (p=< 0.05 to < 0.001). Captopril dose-dependently reduced total and differential WBC counts, improved serum oxidative stress indices, and reduced lung histopathological changes in LPS-treated rats (p<0.05 to p<0.001).
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