The inhibitory effect of pearl grass extract on the pro-inflammatory cytokine TNF-Α, IL-10, and IL-6 levels in LPS-induced acute lung inflammation mice.

Abstract

Pro-inflammatory cytokines TNF-α, IL-6, and IL-10 are involved in the inflammation process of acute lung injury. Thus, inhibiting the upregulation of pro-cytokine inflammation was suggested to be capable of controlling the development of acute lung inflammation.  Previous studies have indicated that Pearl grass extract contains secondary metabolites with potential anti-inflammatory effects. This study determined the impact of pearl grass ethanol extract on the pro-inflammatory cytokine TNF-α, IL-6, and IL-10 of the lipopolysaccharide-induced lung inflammation in mice. A total of 25 mice, 5 of each group were subjected to distilled water without lipopolysaccharide (Normal group), with lipopolysaccharide (Negative control group) and three treatment groups with lipopolysaccharide + pearl grass extract doses 250, 500, and 750 mg/kg BW respectively.  Pearl grass extract was administered orally for 7 consecutive days, and lipopolysaccharide was instilled intranasally. On day eight except for the normal group, all mice were euthanized 72 hours post LPS administration followed by collecting bronchoalveolar-lavage fluid (BALF). TNF-α, and IL-6, levels in the lungs were determined using enzyme-linked immunosorbent assay.  Pearl grass extract at a dose of 250 mg/kg bw significantly reduced TNF-α and IL-6 levels but not IL 10. Our finding indicated the potential effect of pearl grass extract on pro cytokine of acute lung inflammation. This could be a valuable approach to reducing the severity of acute lung inflammation.