Ginger extract attenuates ethanol-induced pulmonary histological changes and oxidative stress in rats.

Alireza Shirpoor,Farzaneh Hosseini Gharalari,Elaheh Heshmati,Yousef Rasmi

doi:10.7555/jbr.31.20160151

Abstract

Chronic ethanol consumption is associated with changes in the function and structure of the lungs. The aim of this study was to investigate the effect of chronic ethanol exposure on the lungs and whether ginger extract mitigated pulmonary abnormalities induced by ethanol in rats. Male Wistar rats were divided into the control group, the ethanol group, and the ethanol plus ginger extract group. Six weeks of ethanol treatment increased the proliferation of lung cells, and induced fibrosis, inflammation and leukocyte infiltration. A significant rise in the level of 8-hydroxydeoxyguanosine, NADPH oxidase, and oxidized low-density lipoprotein was also observed. Ginger extract significantly ameliorated the above changes. These findings indicate that ethanol induces abnormalities in the lungs by oxidative DNA damage and oxidative stress, and that these effects can be alleviated by ginger, which may function as an antioxidant and anti-inflammatory agent.

Highlights

The association between ethanol consumption and lung abnormalities, such as diffuse alveolar damage, impaired gas exchange, pro-inflammatory cytokines release, as well as predisposing factors that increase the incidence of acute respiratory distress syndrome (ARDS) is well known[1,2]
Previous studies demonstrated that exposure to ethanol in experimental models led to oxidative stress that was manifested by a marked decrease in antioxidant glutathione in lung tissues and an increase in NADPH oxidase expression and superoxide generation in the lungs through the renninangiotensin pathway[10,11]
We identified an increase in NADPH oxidase activity, focal polymorphonuclear cell infiltration, as well as fibrosis in rats exposed to ethanol

Summary

Introduction

The association between ethanol consumption and lung abnormalities, such as diffuse alveolar damage, impaired gas exchange, pro-inflammatory cytokines release, as well as predisposing factors that increase the incidence of acute respiratory distress syndrome (ARDS) is well known[1,2]. The oxidative nature of ethanol-induced abnormalities, on the one hand, and the ameliorative or protective effect of antioxidant administration, on the other hand, prompted us to re-examine this theory that maybe the deleterious effect of chronic ethanol consumption on the lungs is entirely or partially mediated by oxidative stress. In the current study, 1we investigated the CLC number: R285.5, Document code: A The authors reported no conflict of interests.

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