Dekspantenol, Sıçanlarda LPS'nin Neden Olduğu Akut Akciğer Hasarında Artan VCAM-1 ve Kaspaz-3 Ekspresyonlarını Azaltarak İnflamasyonu ve Apoptozu İnhibe Eder

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