Fas inhibition attenuates lipopolysaccharide-induced apoptosis and cytokine release of rat type II alveolar epithelial cells |
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Authors: | Xinhua Ma Daomiao Xu Yuhang Ai Guangfeng Ming Shuangping Zhao |
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Institution: | (1) Department of ICU, Xiangya Hospital, Central South University, 410008 Changsha, China; |
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Abstract: | The aim of this study is to investigate whether silencing of Fas could have an influence on type II alveolar epithelial cell
(AEC) apoptosis and inflammatory cytokine production, which prevents alveolar healing after acute lung injury (ALI). Rat primary
type II AECs were isolated by elastase cell dispersion and IgG panning. The cells were transfected with Fas-specific small
interfering RNA (siRNA) followed by treatment with lipopolysaccharide (LPS), Fas ligand (FasL) or both. The effects of siRNA-mediated
silencing of Fas on LPS-induced apoptosis and cytokine release were then assessed. Notably, LPS, either alone or together
with FasL, significantly stimulated type II AEC apoptosis and the release of tumor necrosis factor-alpha (TNF-α) and monocyte
chemoattractant protein 1 (MCP-1) (P < 0.05 versus the control without treatment). Moreover, the effects exerted by both LPS and FasL were considerably counteracted
by pretreatment with Fas-siRNA (P < 0.05 versus treatment with LPS and FasL). In conclusion, inhibition of Fas can diminish LPS-induced apoptosis and inflammatory
cytokine production in type II AECs, and Fas specific siRNAs may have therapeutic potentials for intervention of ALI/ARDS. |
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