Abstract Title:

Epigallocatechin gallate attenuates cardiopulmonary bypass-associated lung injury.

Abstract Source:

J Surg Res. 2016 Apr ;201(2):313-25. Epub 2015 Nov 11. PMID: 27020813

Abstract Author(s):

Bernhard Kasper, Aida Salameh, Miriam Krausch, Philipp Kiefer, Martin Kostelka, Friedrich Wilhelm Mohr, Stefan Dhein

Article Affiliation:

Bernhard Kasper

Abstract:

BACKGROUND: Lung dysfunction constitutes a severe complication after major cardiac surgery with cardiopulmonary bypass (CPB), substantially contributing to postoperative morbidity and mortality. The current possibilities of preventive and therapeutic interventions, however, remain insufficient. We, therefore, investigated the effects of intraoperative application of the antioxidant and anti-inflammatory green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) on CPB-associated lung injury.

MATERIALS AND METHODS: Thirty piglets (8-15 kg) were divided into four groups: sham-operated and saline-treated control group (n = 7); sham-operated and EGCG-treated control group (EGCG-control group; n = 7); CPB group (n = 10); and CPB + EGCG group (n = 6). The CPB groups underwent 120 min of CPB followed by 90 min of recoverytime. In the CPB + EGCG group, EGCG (10 mg/kg body weight) was administered intravenously before and after CPB. Hemodynamic monitoring, blood gas analysis, hematoxylin-eosin staining, and immunohistochemistry of lung tissue were performed.

RESULTS: Histologic examination revealed thickening of the alveolar wall and enhanced alveolar neutrophil infiltration in the CPB group (P < 0.05) compared with those in the control group, which was prevented by EGCG (P < 0.05). In the CPB group, higher formation of poly(ADP-ribose) and nuclear translocation of apoptosis-inducing factor was detected in comparison with those in the control group (P < 0.001), which were both reduced in the CPB + EGCG group (P < 0.001). Compared with the control group, the EGCG-control group showed thickening of the alveolar wall and increased neutrophil infiltration (P < 0.05).

CONCLUSIONS: CPB leads to lung edema, pulmonary neutrophil infiltration, and presumably initiation of poly(ADP-ribose) polymerase-dependent cell death signaling in the lung. EGCG appears to attenuate CPB-associated lung injury, suggesting that this may provide a novel pharmacologic approach.

Study Type : Animal Study

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