Ginsenoside Rd Attenuates Lung Ischemia/Reperfusion Injury in Mice via Regulating Mitochondrial Function

In emergency and critical care medicine, lung ischemia-reperfusion injury is a prevalent disorder, which has significant morbidity and mortality. However, there is still a lack of effective means to block the lung ischemia-reperfusion injury. Established the lung ischemia-reperfusion injury model of mice; lung injury and histological analysis scoring were helpful to assess pathological injury in lung tissue; using an enzyme-linked immunosorbent assay kit, expressed interleukin-6 and interleukin-1 in bronchoalveolar lavage fluids was determined. Seahorse analysis was used to examine the oxygen consumption rate and production of adenosine triphosphate. The expression of mitochondrial function-related genes was detected by real-time polymerase chain reaction; commercially available assay kits used for find the malondialdehyde production and catalase activity; apoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling and protein expression was discovered using Western blotting. Ginsenoside alleviated the pathological changes caused by lung ischemia-reperfusion injury and reduced the lung injury score; ginsenoside Rd therapy reduced inflammatory cell infiltration significantly decreased lung bronchoalveolar lavage fluids interleukin-1 and interleukin-6 levels; ginsenoside Rd also increased the respiratory rate and the adenosine triphosphate production and regulated mitochondrial-related gene expression. Moreover, ginsenoside Rd ameliorated the lung ischemia-reperfusion injury-associated decrease in superoxide dismutase 2 expression, increase in malondialdehyde content and reduction in catalase activity. Additionally, ginsenoside Rd decreased lung ischemia-reperfusion injury-induced apoptosis. Ginsenoside Rd regulates the mitochondrial activity and thus protects against lung ischemia-reperfusion injury.