AI Summary & Key Takeaways
AI InsightThese findings indicate that DEX provides a protective effect against IR-induced liver damage.
📌 3 Key Takeaways
Abstract
Objective Pulmonary ischemia-reperfusion (IR) injury can lead to liver damage through inflammation triggered by hypoxic conditions. Dexpanthenol (DEX), known for its anti-inflammatory properties in organs such as the lung, liver, and kidney, may exert hepatoprotective effects. This study investigates the potential of DEX in mitigating hepatic injury following pulmonary IR. Material and Method A total of 40 rats were randomly allocated into four experimental groups: control, ischemia-reperfusion (IR), IR treated with dexpanthenol (IR+DEX; 500 mg/kg, intraperitoneally, single dose), and DEX alone. Following left thoracotomy, non-traumatic vascular occlusion was performed for 60 min, followed by a 60-min reperfusion period. Upon sacrification, liver tissues were harvested and fixed in formaldehyde for subsequent histopathological and immunohistochemical evaluation. Results Histological evaluation of liver sections from the control and DEX groups revealed normal tissue architecture. In contrast, the IR group exhibited prominent pathological changes, including moderate hyperemia, hepatocellular necrosis, inflammatory cell infiltration, and mild hemorrhage, predominantly around the central veins. Notably, liver sections from the DEX-treated groups demonstrated marked histological improvement compared to the IR group. Immunohistochemical analysis revealed minimal cytoplasmic expression of c-Fos, HIF-1α, and IL-6 in the control group. In contrast, the IR group exhibited a marked increase in the expression of all three markers within liver tissue. DEX treatment notably reduced the expression levels of c-Fos, HIF-1α, and IL-6, suggesting a protective effect against IR-induced hepatic injury. While inflammatory cells and bile duct epithelial cells showed similar expression patterns, hepatocytes were the primary source of these immunoreactive signals. All marker expressions were confined to the cytoplasm. These findings indicate that DEX provides a protective effect against IR-induced liver damage. Conclusion In the context of pulmonary IR, damage is likely to occur not only in lung tissue but also in other secondary organs. This is attributed to the dissemination of immunomodulatory cytokines developed within the tissue through the bloodstream to other organs. DEX, a derivative of pantothenic acid recognized in the literature for its tis-sue-protective effects and known anti-inflammatory properties, mitigates inflammation in liver damage resulting from lung IR injury, as evidenced by alterations and changes in immunological markers.
Özet
Objective Pulmonary ischemia-reperfusion (IR) injury can lead to liver damage through inflammation triggered by hypoxic conditions. Dexpanthenol (DEX), known for its anti-inflammatory properties in organs such as the lung, liver, and kidney, may exert hepatoprotective effects. This study investigates the potential of DEX in mitigating hepatic injury following pulmonary IR. Material and Method A total of 40 rats were randomly allocated into four experimental groups: control, ischemia-reperfusion (IR), IR treated with dexpanthenol (IR+DEX; 500 mg/kg, intraperitoneally, single dose), and DEX alone. Following left thoracotomy, non-traumatic vascular occlusion was performed for 60 min, followed by a 60-min reperfusion period. Upon sacrification, liver tissues were harvested and fixed in formaldehyde for subsequent histopathological and immunohistochemical evaluation. Results Histological evaluation of liver sections from the control and DEX groups revealed normal tissue architecture. In contrast, the IR group exhibited prominent pathological changes, including moderate hyperemia, hepatocellular necrosis, inflammatory cell infiltration, and mild hemorrhage, predominantly around the central veins. Notably, liver sections from the DEX-treated groups demonstrated marked histological improvement compared to the IR group. Immunohistochemical analysis revealed minimal cytoplasmic expression of c-Fos, HIF-1α, and IL-6 in the control group. In contrast, the IR group exhibited a marked increase in the expression of all three markers within liver tissue. DEX treatment notably reduced the expression levels of c-Fos, HIF-1α, and IL-6, suggesting a protective effect against IR-induced hepatic injury. While inflammatory cells and bile duct epithelial cells showed similar expression patterns, hepatocytes were the primary source of these immunoreactive signals. All marker expressions were confined to the cytoplasm. These findings indicate that DEX provides a protective effect against IR-induced liver damage. Conclusion In the context of pulmonary IR, damage is likely to occur not only in lung tissue but also in other secondary organs. This is attributed to the dissemination of immunomodulatory cytokines developed within the tissue through the bloodstream to other organs. DEX, a derivative of pantothenic acid recognized in the literature for its tis-sue-protective effects and known anti-inflammatory properties, mitigates inflammation in liver damage resulting from lung IR injury, as evidenced by alterations and changes in immunological markers.