N-acetylcysteine attenuates cardiopulmonary bypass-induced lung injury in dogs

Xianfeng Qu,Xiaofei Wang,Qianyu Li,Dongguo Wang,Xiaoping Yang

doi:10.1186/1749-8090-8-107

Xianfeng Qu, Xiaofei Wang + Show 3 more

Open Access

https://doi.org/10.1186/1749-8090-8-107

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Abstract

BackgroundCardiopulmonary bypass (CPB) is usually associated with inflammatory response that leads to various degrees of organ dysfunction in multiple systems, including lung injury. Our previous study showed that transforming growth factor beta1 (TGFβ1) was involved in CPB-induced lung injury. N-acetylcysteine (NAC) is an antioxidant and is able to prevent CPB-induced pneumocyte apoptosis through scavenging radical. Therefore, we investigated whether NAC may attenuate CPB-induced lung injury by inhibiting TGFβ1 expression.MethodsFifty-four 18 to 24-month-old mongrel dogs (15–16 kg) were randomly divided into control group, CPB group and NAC group (n = 18). Six dogs in each group were killed prior to, as well as 30 and 60 minutes after the operation (T0, T1 and T2). Lung injury was evaluated by hematoxylin and eosin (H&E) staining. Respiratory index (RI), oxygenation index (OI), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the lung were determined at each time point. TGFβ1 expression was determined using real time RT-PCR and immunohistochemistry.ResultsA serious lung injury was observed after CPB in dogs. RI and MDA content were increased significantly after CPB, whereas OI and SOD activity were decreased. H&E staining showed that NAC treatment obviously attenuated CPB-induced lung injury. NAC treatment upregulated OI and SOD activity and downregulated RI and MDA content in the lung tissues of dogs after CPB. Treatment with NAC significantly suppressed the TGFβ1 expression in the lung tissues at both mRNA and protein levels.ConclusionOur results suggest that NAC is a potent agent against CPB-induced acute lung injury through inhibiting TGFβ1 expression.

Highlights

Cardiopulmonary bypass (CPB) is usually associated with inflammatory response that leads to various degrees of organ dysfunction in multiple systems, including lung injury
The Respiratory index (RI) values of NAC group were lower and the oxygenation index (OI) values of NAC group were higher at T1 and T2 time points than those of CPB group, respectively
NAC inhibited the Transforming growth factor beta1 (TGFβ1) expression in the lung tissues To investigate the effect of NAC on the expression of TGFβ1 in lung tissues, we performed RT-PCR and Discussions In the present study, we investigated the effect of NAC on CPB-induced acute lung injury

Summary

Introduction

Cardiopulmonary bypass (CPB) is usually associated with inflammatory response that leads to various degrees of organ dysfunction in multiple systems, including lung injury. N-acetylcysteine (NAC) is an antioxidant and is able to prevent CPB-induced pneumocyte apoptosis through scavenging radical. NAC is able to alleviate lung reperfusion injury induced by deep hypothermic circulatory arrest through scavenging oxygen free radicals [18]. It can reduce the pulmonary vascular resistance index and decrease the incidence of lung injury after off-pump coronary artery bypass surgery [19]. In view of the important role of TGFβ1 during the progression of acute lung injury, the objective of this work was to investigate whether NAC could exert a protective effect on CPB-induced acute lung injury through inhibiting the expression of TGFβ1

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