Modulatory effects of 17?-estradiol on acute lung inflammation after total occlusion of the descending aorta in male rats

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5
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article
Data de publicação
2022
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INTERNATIONAL IMMUNOPHARMACOLOGY, v.113, article ID 109311, 9p, 2022
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As a consequence of systemic inflammation caused by ischemia and reperfusion (I/R) due to aortic occlusion, the lungs can exhibit increased microvascular permeability, local release of pro-inflammatory mediators, and leukocyte infiltration. Lung tissue infiltration by activated neutrophils is followed by acute respiratory distress syndrome, which is linked to acute pulmonary microvascular damage, high mortality rates, and organ dysfunction. Previous studies have demonstrated that female sex hormones modulate the inflammatory response and that prophylactic treatment with 178-estradiol (E2) can prevent fatalities and preserve mesenteric perfusion and intestinal integrity after ischemia/reperfusion induced by aortic occlusion. In this study, we focused on the protective effects of estradiol after aortic ischemia/reperfusion by evaluating lung injury and endothelial al-terations. Upon anesthesia and mechanical ventilation, male rats were subjected to aortic occlusion for 20 min, followed by 2 h of reperfusion. In parallel, one group of rats received a single injection of estradiol (280 mu g/kg, i. v.) 30 min before ischemia. We observed increased serum concentrations of IL-18, IL-6 and IL-10 in the I/R rats and E2 was able to reduce them. E2 effects after 2 h of reperfusion resulted mainly in decreasing of edema, iNOS expression and preventing leukocyte infiltration. Overall, our data indicate that estradiol might be a supple-mentary approach to deal with systemic processes and lung deterioration.
Palavras-chave
Ischemia and Reperfusion, 17&beta, -estradiol, Lung inflammation, iNOS
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