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<p><span style="color: rgb(17, 17, 17); font-family: Poppins; font-size: 14px;">This study aims to investigate the effects of Dexpanthenol (Dex), a stable alcoholic analogue of D-pantothenic acid which has anti-oxidant, antiapoptotic, and antiinflammatory properties, on lipopolysaccharide (LPS)-induced lung damage via caspase-3 (cas-3) and vascular cell adhesion molecule-1 (VCAM-1) levels. According to the experimental plan of study, thirty-two Wistar Albino rats were distributed randomly into four groups as control, LPS (5 mg/kg, intraperitoneally (i.p), single dose), LPS (30 minutes before last Dex treatment) + Dex (500 mg/kg, i.p, for 3 days) and Dex. After six hours of LPS application, lung tissues of the rats were taken for histopathological, immunohistochemical and biochemical examinations. According to results of the study, LPS caused hyperemia, neutrophil leukocyte chemotaxis and thickened septal tissue on lung. Inducing inflammation by increasing VCAM-1 expression and triggered apoptosis by increasing cas-3 expression in lung tissue. In addition, LPS decreased total antioxidant status levels, which is a marker of anti-oxidant capacity, and increased oxidative stress index and total oxidant status values, which are indicators of oxidative stress. Dex has shown its effect by reversing all these alterations and normalizing the values. These results suggest that Dex can be used as a preservative to reduce LPS-induced acute toxicity in the lung.</span><br></p> |
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