Background Excessive deposition of extraceUular matrix （ECM） in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative path...Background Excessive deposition of extraceUular matrix （ECM） in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative pathways, particularly in the in vivo setting. The renal protective effect of these pathways on matrix accumulation has not been fully elucidated. The present study was understaken to investigate the activity of matrix metalloproteinase-2 （MMP-2）, the expression of MMP-2 and tissue inhibitor of metalloproteinase-2 （TIMP-2） in kidney tissues of diabetic rats, and to explore the degradative pathway of type Ⅳ collagen （Ⅳ-C） and the renal protective effects of ACE inhibition- benazepril.展开更多
基金This study was supported by a grant from the Natural Science Foundation of Shandong Province (No. Y2002C35).
文摘Background Excessive deposition of extraceUular matrix （ECM） in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative pathways, particularly in the in vivo setting. The renal protective effect of these pathways on matrix accumulation has not been fully elucidated. The present study was understaken to investigate the activity of matrix metalloproteinase-2 （MMP-2）, the expression of MMP-2 and tissue inhibitor of metalloproteinase-2 （TIMP-2） in kidney tissues of diabetic rats, and to explore the degradative pathway of type Ⅳ collagen （Ⅳ-C） and the renal protective effects of ACE inhibition- benazepril.
