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. 2017 Aug 1;10(8):9021-9028.
eCollection 2017.

Sulforaphane attenuates acute lung injury by inhibiting oxidative stress via Nrf2/HO-1 pathway in a rat sepsis model

Bo Zhao  1 , Wenwei Gao  2 , Xiang Gao  3 , Yan Leng  1 , Min Liu  1 , Jiabao Hou  1 , Yang Wu  1
Affiliations

Sulforaphane attenuates acute lung injury by inhibiting oxidative stress via Nrf2/HO-1 pathway in a rat sepsis model

Bo Zhao et al. Int J Clin Exp Pathol. .

Abstract

Sulforaphane (SFN), an antioxidant derived from cruciferous vegetables, exerts antioxidant capacity and protects organ against oxidative damage. However, the effects of SFN on sepsis-induced acute lung injury (ALI) have not been determined. The aim of this study was to investigate the effect of SFN in sepsis-induced ALI and the role of Nrf2/HO-1 in this process. Rats were subjected to either sham-operated or cecal ligation and puncture-induced sepsis without or with SFN. Pulmonary oxidative stress was significantly increased (reduced SOD activity, enhanced 8-OHdG concentration, elevated 15-F2t-isoprostane level, and enhanced 4-HNE expression) in sepsis that were associated with elevated lung injuries (Increased lung injury index, elevated lung water content, and reduced endothelial barrier integrity). Supplementation of SFN significantly enhanced Nrf2 and HO-1 protein expression in the lungs in sepsis. Further, SFN dose-dependently reduced pulmonary oxidative stress and attenuated lung injuries in sepsis. However, these beneficial effects of SFN were reduced by HO-1 inhibition. Therefore, we concluded that SFN attenuated ALI in sepsis by reducing oxidative stress through activating Nrf2/HO-1.

Keywords: Sulforaphane; acute lung injury; oxidative stress; sepsis.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Sulforaphane does-dependently attenuated sepsis-induced ALI. A. H&E-stained sections of lungs (×400); B. Lung injury index; C. Lung water content. Date are mean ± SEM, n=8/group, *P<0.05 vs. Sham, #P<0.05 vs. CLP. CLP: Cecal ligation puncture; SFN: Sulforaphane.
Figure 2
Figure 2
Sulforaphane reduced pulmonary oxidative stress induced by sepsis. A. Superoxide dismutase (SOD) activity in the lungs assessed by using an enzyme-linked immunoassay kit; B. 8-OHdG concentration in the lungs determined by using an enzyme-linked immunoassay kit; C. 15-F2t-isoprostane in the lung tissues was measured by using an enzyme-linked immunoassay kit; D. Visualization of expression of 4-hydroxynonenal (4-HNE). Date are mean ± SEM, n=8/group, *P<0.05 vs. Sham, #P<0.05 vs. CLP. CLP: Cecal ligation puncture; SFN: Sulforaphane.
Figure 3
Figure 3
Effect of sulforaphane on the integrity of the endothelial barrier in the lung tissue after sepsis and the Nrf2/HO-1 pathway activation. A-C. Protein expression of claudin-1, occludin, and ZO-1. D. Protein expression of nuclear Nrf2; E. Protein expression of HO-1. Date are mean ± SEM, n=8/group, *P<0.05 vs. Sham, #P<0.05 vs. CLP. CLP: Cecal ligation puncture; SFN: Sulforaphane.
Figure 4
Figure 4
HO-1 inhibition abolishedpulmonary protective effects of sulforaphane. A, B. Representative images and quantitation of HO-1 protein expression; C. H&E-stained sections of lungs (×400); D. Lung injury index; E. 15-F2t-isoprostane in the lung tissues was measured by using an enzyme-linked immunoassay kit; F. Superoxide dismutase (SOD) activity in the lungs assessed by using an enzyme-linked immunoassay kit. Date are mean ± SEM, n=8/group, *P<0.05 vs. Sham, #P<0.05 vs. CLP. CLP: Cecal ligation puncture; SFN: Sulforaphane.
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