Abstract:ObjectiveBy observing the influence of PKCβI membrane translocation and protein expression level in pulmonary artery Smooth muscle cells and Fibroblasts of chronic hypoxia-induced rat pulmonary hypertension, discuss the function of PKCβI in process of chronic hypoxia-induced rat pulmonary hypertension preliminary.MethodsChronic atmospheric pressure hypoxic PH model rats were established. Male SD rats were randomLy divided into six groups,and exposed to normoxia control or to normoxia hypoxia for 1d,3d,7d,14d and 21d to induce pulmonary hypertension. Western blot and immunohistochemistry were used to detect the expression of PKCβI membrane translocation and protein expression level in pulmonary artery Smooth muscle cells and Fibroblasts of chronic hypoxia-induced rat pulmonary hypertension. Results(1) RVSP and RV/(LV+S) increased significantly than normal control groups(P<0.05),rats pulmonary vascular obvious thickening after chronic hypoxia 3d,7d,14d and 21d. (2).PKCβI was expressed in rat pulmonary artery Smooth muscle cells and Fibroblasts, and its protein expressions decreased at 14d after chronic hypoxia than normal control groups(P<0.05).ConclusionsPKCβI protein expression is involved in the development of pulmonary vascular remodeling of chronic hypoxia-induced rat PH.