The Effects of N-acetylcystein and Epigallocatechin-3-Gallate in Ischemia-Reperfusion Injury of Rat Lungs / 대한이식학회지

ABSTRACT

BACKGROUND: Ischemia-reperfusion injury (IRI) is a major cause of early graft dysfunction after lung transplantation. The aim of this study was to assess the effects of N-acetylcystein (NAC) and epigallocatechin-3-gallate (EGCG) on IRI of rat lungs. METHODS: Sprague-Dawley rats were divided into four groups. Sham group (n=6) did not receive IRI. Rats in the control group (n=6), NAC group (n=6), and EGCG group (n=6) were treated with an intraperitoneal injection of normal saline, NAC, and EGCG, respectively, prior to IRI. In the latter three groups, IRI was induced by clamping the left pulmonary artery, vein, and main stem bronchus for a period of 60 minutes. After ischemia, reperfusion and ventilation of the lung was allowed for a period of 180 minutes. The expression levels of inducible nitric oxide synthase (iNOS), hemeoxygenase-1 (HO-1), AMP-activated protein kinase-alpha (AMPK), and caveolin-1 in lung tissues were evaluated by Western blot. The pathological findings and the extent of pulmonary edema after IRI were compared among the groups. RESULTS: The expression levels of iNOS decreased in the Sham and EGCG groups. The expression level of HO-1 was significantly higher in the EGCG group (P=0.0001). Although the expression levels of AMPK and caveolin-1 showed no differences, the extent of phosphorylation of AMPK and caveolin-1 was higher in the EGCG and NAC groups, respectively. In hematoxylin-eosin staining, the lungs in the NAC and EGCG groups showed fewer alveolar injuries and less hemorrhagic congestion compared with the control group. CONCLUSIONS: NAC and EGCG enhanced the phosphorylation of caveolin-1 and AMPK, respectively, and attenuated lung injury induced by ischemia-reperfusion.