To explore the role of HIF-1α in PM_2.5-induced lung injury.

The rat model of lung injury induced by tracheal aerosol PM_2.5 suspension was established, HIF-1α expression and lung injury under different PM_2.5 exposure doses were investigated by western blot, pathological section, ROS staining, TUNEL staining and ELISA. An animal model was constructed to inhibit HIF-1α expression, and the mechanism of HIF-1α in lung injury induced by PM_2.5 exposure was investigated by western blot, immunofluorescence and ELISA.

PM_2.5 exposure causes pathological damage, increases ROS level, apoptosis rate and wet-dry ratio of lung tissue, promotes the count of various inflammatory cells and the levels of inflammatory factors IL-6 and TNF-α in BALF, and activates the protein expression of HIF-1α in lung tissue, the above effects are related to PM_2.5 exposure concentration. Inhibition of HIF-1α can reduce lung inflammation by decreasing NF-κB expression in lung tissue and the level of inflammatory factors in BALF. Inhibition of HIF-1α can reduce lung tissue edema by decreasing VEGF expression in lung tissue, albumin level in BALF and lung tissue wet-dry ratio.

PM_2.5 aggravates lung tissue inflammation, pulmonary vascular permeability and pulmonary edema by activating two pathways: HIF-1α-NF-κB-inflammatory cells(AMs, NEUs)/inflammatory factors(IL-6, TNF-α)-lung tissue inflammation and HIF-1α-VEGF-pulmonary vascular permeability-pulmonary edema.