Abstract
BackgroundPleurotus giganteus (Berk. Karunarathna and K.D. Hyde), has been used as a culinary mushroom and is known to have medicinal properties but its potential as an anti-inflammatory agent to mitigate inflammation triggered diseases is untapped. In this study, the molecular mechanism underlying the protective effect of ethanol extract of P. giganteus (EPG) against lipopolysaccharide (LPS) and combination of LPS and hydrogen peroxide (H2O2)-induced inflammation on RAW 264.7 macrophages was investigated.MethodThe effect of EPG on nitric oxide (NO) production as an indicator of inflammation in RAW 264.7 macrophages was estimated based on Griess reaction that measures nitrite level. The expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), NF-kB activating protein (NKAP), signal transducer and activator of transcription 3 protein (STAT 3) and glutathione peroxidase (GPx) genes were assessed using real time reverse transcription polymerase chain reaction (RT-PCR) approach.ResultsEPG (10 μg/ml) showed the highest reduction in the LPS-induced NO production in RAW 264.7 macrophages and significantly suppressed (p < 0.05) the expression iNOS, STAT 3 and COX-2. There was a significant increase (p < 0.05) in combination of LPS and H2O2- induced iNOS production when compared to the LPS-induced iNOS production in RAW 264.7 macrophages and this concurred with the NO production which was attenuated by EPG at 10 μg/ml. A significant (p < 0.05) down regulation was observed in the combination of LPS and H2O2-induced iNOS and GPx expression by EPG.ConclusionsOur data suggest that the anti-inflammatory activity of EPG is mediated via the suppression of the STAT 3 and COX-2 pathways and can serve as potential endogenous antioxidant stimulant.
Highlights
extract of P. giganteus (EPG) (10 μg/ml) showed the highest reduction in the LPS-induced nitric oxide (NO) production in RAW 264.7 macrophages and significantly suppressed (p < 0.05) the expression inducible nitric oxide synthase (iNOS), STAT 3 and COX-2
There was a significant increase (p < 0.05) in combination of LPS and Hydrogen peroxide (H2O2)- induced iNOS production when compared to the LPS-induced iNOS production in RAW 264.7 macrophages and this concurred with the NO production which was attenuated by EPG at 10 μg/ml
A significant (p < 0.05) down regulation was observed in the combination of LPS and H2O2induced iNOS and glutathione peroxidase (GPx) expression by EPG
Summary
Macrophages play a crucial role in counteracting the invasion of pathogens by releasing inflammatory mediators such as prostaglandin and pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1α and IL-1β). These macrophages act upon the stimuli by a process called phagocytosis. The process of recovering the cellular functions and structure back to its normal condition is called the acute phase of inflammation which is crucial to our body These inflammatory mediators are essential in the defence mechanism, their overproduction causes chronic inflammation and the continuous destruction can be detrimental to tissues. Chronic inflammation has been linked to the pathogenesis of various diseases such as diabetes [3], Alzheimer’s [4], cardiovascular disease [5], and cancer [6] and these diseases have been shown to be the leading causes of death
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