Tryptophan decreases the intensity of lipopolysaccharide-induced acute lung injury in a rat model.

Abstract

Sepsis is a severe clinical condition that is a result of the cellular and biochemical response to infection. The present study evaluated the therapeutic potential of tryptophan against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Rats were grouped into sham, control (ALI), and ALI + 1, 25, and 50mg/kg body weight L-tryptophan. Supplementation with 1, 25, and 50mg/kg L-tryptophan reduced the total protein content by 4.9%, 33.4%, and 64.5%; the levels of neutrophils (12.5%, 31.8%, and 65.1%), lymphocytes (15.1%, 41.7%, and 63.3%), total cells (12.6%, 42.4%, and 65.7%); lipid peroxidation (9.4%, 28.4%, and 68.7%); myeloperoxidase levels (12.1%, 33.4%, and 68.2%); migration inhibitory factor (12.7%, 39.5%, and 68.2%), interleukin (IL)-8 (5.5%, 46.8%, and 78.5%), tumor necrosis factor (TNF)-α (10.8%, 39.8%, and 72.2%), respectively. Supplementation with 1, 25, and 50mg/kg L-tryptophan reduced mRNA expression of TNF-α (4.5%, 21.8%, and 41.8%), IL-1β (5.2%, 17.9%, and 46.2%); and the protein expression of TNF-α (2.8%, 15.2%, and 35.7%) and IL-1β (5.2%, 15.6%, and 28.6%), respectively. It also reduced glutathione (to near normal levels), neutrophilic infiltration and edema, and the wet/dry ratio of lung tissue. It significantly increased catalase, superoxide dismutase, glutathione peroxidase levels, as well as the partial pressure of oxygen (PaO2) by 21.9%, 52.8%, and 87.4%, respectively. Altogether, our results suggest that supplementation with L-tryptophan has a strong protective effect against LPS-induced ALI.