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作 者:SUN Shu-zhen WANG Yi LI Qian TIAN Yong-jie LIU Ming-hua YU Yong-hui
机构地区:[1]Department of Pediatrics, Shandong Provincial Hospital, ShandongUniversity, Jinan 250021, China
出 处:《Chinese Medical Journal》2006年第10期814-821,共8页中华医学杂志(英文版)
基 金:This study was supported by a grant from the Natural Science Foundation of Shandong Province (No. Y2002C35).
摘 要: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.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.
关 键 词:angiotensin converting enzyme inhibitors diabetic nephropathy renal function matrix metalloproteinase-2 tissue inhibitor of metalloproteinase-2
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