Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Abstract

The effects of S-ethyl cysteine (SEC) and S-methyl cysteine (SMC) on lipopolysaccharide (LPS)-induced acute lung injury in mice were examined. Eight hours after LPS challenge, SEC or SMC was supplied in drinking water at 0.5% or 1% for 3 days. LPS increased lung myeloperoxidase activity, neutrophil counts and edema. SEC or SMC post-intake attenuated these events. SEC or SMC suppressed LPS-induced lung expression of cyclooxygenase-2, nuclear factor-κB and mitogen-activated protein kinase, and lowered the generation of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin E₂. LPS enhanced the expression of p47(phox), gp91(phox), Bax and cleaved caspase-3, and increased the production of reactive oxygen species in the lung. SEC or SMC post-intake reversed these alterations. These findings suggest that these agents could protect the lung through their anti-inflammatory, anti-oxidative and anti-apoptotic activities.

Keywords: LPS; S-ethyl cysteine; S-methyl cysteine; inflammation; lung.

Figure 1

Lung MPO (myeloperoxidase) activity (a); and neutrophil count (b) of mice in normal group, LPS (lipopolysaccharide) group, LPS + low SEC (S-ethyl cysteine) group, LPS + high SEC group, LPS + low SMC (S-methyl cysteine) group and LPS + high SMC group after 3-day treatments. Data are mean ± SD (standard deviation), n = 10. ^a–e Means among bars without a common letter differ, p < 0.05.

Figure 1

Lung MPO (myeloperoxidase) activity (a); and neutrophil count (b) of mice in normal group, LPS (lipopolysaccharide) group, LPS + low SEC (S-ethyl cysteine) group, LPS + high SEC group, LPS + low SMC (S-methyl cysteine) group and LPS + high SMC group after 3-day treatments. Data are mean ± SD (standard deviation), n = 10. ^a–e Means among bars without a common letter differ, p < 0.05.

Figure 2

Lung expression of COX-2, NF-κB and MAPK of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−e Means among bars without a common letter differ, p < 0.05.

Figure 2

Lung expression of COX-2, NF-κB and MAPK of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−e Means among bars without a common letter differ, p < 0.05.

Figure 3

Lung expression of p47^phox, gp91^phox, GPX, GR and catalase of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−e Means among bars without a common letter differ, p < 0.05.

Figure 3

Lung expression of p47^phox, gp91^phox, GPX, GR and catalase of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−e Means among bars without a common letter differ, p < 0.05.

Figure 4

Lung expression of Bcl-2, Bax and cleaved caspase-3, and ratio of Bcl-2/Bax of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−d Means among bars without a common letter differ, p < 0.05.

Figure 4

Lung expression of Bcl-2, Bax and cleaved caspase-3, and ratio of Bcl-2/Bax of mice in normal group, LPS group, LPS + low SEC group, LPS + high SEC group, LPS + low SMC group and LPS + high SMC group after 3-day treatments. Data are mean ± SD, n = 10; ^a−d Means among bars without a common letter differ, p < 0.05.

Figure 5

Schematic diagram for lung protein of SEC or SMC against LPS.