Expression of vascular endothelial growth factor and hypoxia-inducible factor 1α in rat traumatic lung injury

Hypoxia-inducible factor 1α (HIF-1α) is an important transcription factor in mediating oxygen homeostasis that can regulate vascular endothelial growth factor (VEGF) gene transcription. HIF-1α can induce neovascularization in ischemic injury. This research observed HIF-1α and VEGF expression in traumatic lung injury (TLI) to discuss their correlation. Healthy male SD rats at 7-week old were randomly divided into control (A) and traumatic group (B). TLI model was established by multi-function small biological tapping machine. Abbreviated injury scale (AIS), respiration, blood pressure (BP), and heart rate were monitored. Lung tissue was extracted at 6, 24, 48, 72, and 96 hours after injury to observe the pathological morphology. Myeloperoxidase (MPO) was measured by spectrophotometry. Pulmonary microvascular permeability was detected by fluorescence spectrophotometry. VEGF protein was tested by ELISA. HIF-1α protein expression was determined by Western blot. MPO activity, pulmonary microvascular permeability, VEGF, and HIF-1α protein expression were significantly higher at 6, 24, 48, 72, and 96 hours after injury compared with group A (P < 0.05). MPO activity reached peak at 24 h, microvascular permeability reached peak at 6 h, and VEGF and HIF-1α reached peak at 48 h after injury. They gradually decreased after that and got close to pre-injury level. VEGF and HIF-1α protein expression presented positive correlation at different time points (r = 0.759, P < 0.05). HIF-1α and VEGF protein elevated after TLI. HIF-1α may protect cell tolerance to hypoxia and promote injured vascular repair and regeneration through regulating VEGF expression.