Activation of the Peroxisome Proliferator-Activated Receptor Preventing he Monocrotaline-Induced Pulmonary Hypertension

The purpose of this study was to investigate the role of peroxisome proliferator-activated receptor gamma (PPARγ) in the development of the monocrotaline (MCT)- induced pulmonary hypertension. Rosiglitazone (TZD) was used to activate the PPARγin this study. Sixty-four Wistar rats (BW = 114.1 ±1.2 g) were divided into five groups: control, MCT, MCT+vehicle (VEH, 15% alcohol), MCT+TZD, and TZD. Rats in the control group received injection of 0.5 ml saline intraperitoneally. Pulmonary hypertension was induced by one bolus injection of MCT (60 mg/kg, sc). Two weeks after MCT treatment, rats were daily treated with either 0.5 ml of 15% alcohol in the MCT+VEH group or TZD (10 mg/kg, ip) in the MCT+TZD group. In the TZD group, the same doses of TZD were given in the saline-treated rats on the corresponding days of the MCT+TZD group. Pulmonary arterial blood pressures were measured on the 22nd day post MCT. Comparing to the control group, the MCT administration caused significant increases in the pulmonary arterial pressure as well as the weight ratio of right ventricle (RV) to the sum of left ventricle and septum (LV+S), and the thickness of the vessel walls, indicating the development of pulmonary hypertension. The TZD treatment significantly attenuated the severity of pulmonary hypertension. However, the endogenous antioxidant enzymes in lung tissues, including superoxide dismutase, glutathione and catalase, were in similar levels among all groups. Therefore, the PPARγattenuated pulmonary hypertension may not be related to the antioxidant pathway.

並列關鍵字

pulmonary hypertension ； monocrotaline ； peroxisome proliferator-activated receptor γ ； rosiglitazone ； superoxide dismutase ； glutathione ； catalase

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