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