The Pantothenic Acid Derivative Dexpanthenol Attenuates Liver Injury Induced by Lung Ischemia- Reperfusion Through Its Anti-Inflammatory Effect

ObjectivePulmonary ischemia-reperfusion (IR) injury can leadto liver damage through inflammation triggered byhypoxic conditions. Dexpanthenol (DEX), known forits anti-inflammatory properties in organs such as thelung, liver, and kidney, may exert hepatoprotectiveeffects. This study investigates the potential of DEX inmitigating hepatic injury following pulmonary IR.Material and MethodA total of 40 rats were randomly allocated into fourexperimental groups: control, ischemia-reperfusion(IR), IR treated with dexpanthenol (IR+DEX; 500mg/kg, intraperitoneally, single dose), and DEXalone. Following left thoracotomy, non-traumaticvascular occlusion was performed for 60 min,followed by a 60-min reperfusion period. Uponsacrification, liver tissues were harvested and fixed informaldehyde for subsequent histopathological andimmunohistochemical evaluation.ResultsHistological evaluation of liver sections from thecontrol and DEX groups revealed normal tissuearchitecture. In contrast, the IR group exhibitedprominent pathological changes, including moderatehyperemia, hepatocellular necrosis, inflammatorycell infiltration, and mild hemorrhage, predominantlyaround the central veins. Notably, liver sectionsfrom the DEX-treated groups demonstrated markedhistological improvement compared to the IR group.Immunohistochemical analysis revealed minimalcytoplasmic expression of c-Fos, HIF-1α, and IL-6 inthe control group. In contrast, the IR group exhibiteda marked increase in the expression of all threemarkers within liver tissue. DEX treatment notablyreduced the expression levels of c-Fos, HIF-1α, andIL-6, suggesting a protective effect against IR-inducedhepatic injury. While inflammatory cells and bile ductepithelial cells showed similar expression patterns,hepatocytes were the primary source of theseimmunoreactive signals. All marker expressions wereconfined to the cytoplasm. These findings indicate thatDEX provides a protective effect against IR-inducedliver damage.ConclusionIn the context of pulmonary IR, damage is likely to occurnot only in lung tissue but also in other secondaryorgans. This is attributed to the dissemination ofimmunomodulatory cytokines developed within thetissue through the bloodstream to other organs. DEX,a derivative of pantothenic acid recognized in the literaturefor its tis-sue-protective effects and knownanti-inflammatory properties, mitigates inflammationin liver damage resulting from lung IR injury, as evidencedby alterations and changes in immunologicalmarkers.