Roles of Nrf2/HO ‐1 and HIF‐1α/VEGF in lung tissue injury and repair following cerebral ischemia/reperfusion injury

CIRI can lead to remote organ injury in the lungs. The Nrf2/HO ‐1 antioxidative stress pathway minimizes pulmonary free radical injury, and HIF‐1α/VEGF advances angiogenesis and repair of the alveolar–capillary barrier. These findings provide a theoretical basis for clinical treatment. AbstractCerebral ischemia/reperfusion injury (CIRI) leads to injury in distant organs, most commonly the lungs, although limited studies have examined self ‐protective mechanisms during CIRI‐induced lung injury. Here, we investigated self‐protective mechanisms that attenuate stress‐related injury and promote the angiogenetic repair of epithelial function during CIRI‐induced lung injury by measuring nuclear factor erythroid‐related factor 2 (Nrf2) and hypoxia‐inducible factor‐1α (HIF‐1α) levels. A CIRI model was established in male Sprague–Dawley rats by blocking the middle cerebral artery. Rats were divided into five subgroups based on the reperfusion time (6, 12, 24, 48, and 72 hr). Lung injury was assessed using a semiqu antitative score and a thiobarbituric acid‐based method of determining malonaldehyde production. Lung tissue angiogenesis was detected by CD34 and CD31 immunolabeling. Changes in Nrf2, heme oxygenase‐1 (HO‐1), HIF‐1α, vascular‐endothelial growth factor (VEGF), phosphatidylinositol 3‐kin ase (PI3K), extracellular‐regulated kinase1/2 (ERK1/2), and phospho‐ERK1/2 (p‐ERK1/2) protein‐ and mRNA‐expression levels were measured by...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: RAPID COMMUNICATION Source Type: research