ABSTRACT. This study investigated the effects of angiotensin II (AngII) intervention, using captopril and losartan, on the expression of matrix metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and collagen in rats with pulmonary hypertension, in an effort to understand mechanisms underlying pulmonary vascular remodeling. A total of 40 male Sprague-Dawley rats were randomly divided into normal group, model group, captopril group, and losartan group. After 5 weeks, the mean pulmonary arterial pressure (mPAP), right ventricular index, and neointima formation in each group were determined. Immunohistochemical analysis was performed to determine the degree of pulmonary arterial muscularization as well as MMP-2, MMP-9, and TIMP-1 protein expression in lung tissue. Real-time fluorescent quantitative PCR was 1707-1717 (2015) used to detect MMP2, MMP9, TIMP1, COL1A1, and COL4A1 mRNA expression. Picro-sirius red staining was performed to detect collagen protein expression. Neointima formation was observed in the model group. Moreover, the mPAP, right ventricular index, degree of arterial muscularization, and collagen deposition, as well as mRNA and protein expression of MMP2, MMP9, and TIMP1 were significantly higher than those in the other groups (P < 0.05). The mPAP, right ventricular index, degree of arterial muscularization, and mRNA and protein expression in the captopril and losartan groups were significantly decreased compared with those of the model group (P < 0.05). AngII regulates MMP-2, MMP-9, and TIMP-1 expression and affects collagen deposition. Thus, this hormone is involved in pulmonary vascular remodeling, indicating a possible mechanism that can be targeted in pulmonary hypertension intervention.

ABSTRACT. This study aimed to determine whether abnormal apoptosis is present in acetabular cartilage in early developmental dislocations of the hip (DDH), and if so, whether it is correlated with the expression of caspase-3 and Bcl-2. DDH was induced in 24 4-week-old New Zealand white rabbits. Acetabular cartilage specimens from the experimental and control groups were stained with hematoxylin and eosin (H&E). Animals from the experimental group developed acetabular dysplasia. Apoptotic chondrocytes were observed by ultrastructural electron microscopy and H&E. TUNEL assays revealed significantly greater acetabular chondrocyte apoptosis in the treated samples as compared to the control. Significantly higher caspase-3 expression and lower Bcl-2 expression were also measured in the DDH group compared with the control. We conclude that excessive apoptosis does occur in acetabular cartilage with DDH, and is positively correlated with high caspase-3 expression as well as low Bcl-2 expression.