Protective effect of Apremilast against LPS-induced acute lung injury via modulation of oxidative stress and inflammation

Abstract

Lung injuries are attributed due to exposure to Drugs or chemicals. One of the important challenging situations for the clinicians is to manage treatments of different diseases with acute lung injury (ALI). The objective of this study was to investigate the possible protective mechanisms and action of a novel Phosphodiesterase-4 inhibitor "Apremilast" (AP) in lipopolysaccharide (LPS)-induced lung injury. Blood sample from each animals were collected in a vacuum blood collection tube. The rat lungs were isolated for oxidative stress assessment, western blot analysis and their mRNA expressions using RT-PCR. Exposure of LPS in rats causes significant increase in oxidative stress, activates the pro-inflammatory cytokines release like tissue necrotic factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), modulated gene expression, protein expression and histopathological changes which were reversed by administration of AP. Finding of the research enlighten the protective role of AP against LPS-induced ALI.

Keywords: Acute lung injury; Apremilast; Lipopolysaccharides; Oxidative stress; mRNA expressions.

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MDA.

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GSH.

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GR.

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TNF-α.

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IL-6.

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IL-1β.

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TNF-α.

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GST.

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AKT1.

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ERK.

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NF-κB p65.

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IκB-α.

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LPS= Lipopolysaccharides: AP= Apremilast: DEX= Dexamethasone: IkB-α = Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha.