Targeting heme oxygenase-1 in early diabetic nephropathy in streptozotocin-induced diabetic rats

被引：16
作者：
El Gheit, R. Abo [1 ]
Emam, M. N. [1 ]
机构：
[1] Tanta Univ, Dept Physiol, Fac Med, Mohamed Adel Salam Awara St, Tanta 31511, Egypt
来源：
PHYSIOLOGY INTERNATIONAL | 2016年 / 103卷 / 04期
关键词：
diabetic nephropathy; heme oxygenase; cobalt protoporphyrin; zinc protoporphyrin IX; renal hydroxyprolin; SPONTANEOUSLY HYPERTENSIVE-RATS; ENHANCES INSULIN SENSITIVITY; NECROSIS-FACTOR-ALPHA; FACTOR-KAPPA-B; CARBON-MONOXIDE; OXIDATIVE STRESS; IN-VIVO; VENTRICULAR-FIBRILLATION; GLUCOSE-METABOLISM; GLOMERULAR INJURY;
D O I：
10.1556/2060.103.2016.4.001
中图分类号：
Q4 [生理学];
学科分类号：
071003 ;
摘要：
Diabetic nephropathy (DN) is one of the most common microvascular diabetic complications. This study was designed to evaluate the possible protective effect and underlying mechanisms of HO-1 induction in streptozotocin (STZ)-induced early DN in rats. The diabetic rats were divided into three groups: STZ-diabetic, cobalt protoporphyrin (CoPP)-treated diabetic, and zinc protoporphyrin IX (ZnPP)-treated diabetic groups. Compared to the STZ-diabetic group, CoPP-induced HO-1 upregulation improved the diabetic state and renal functional parameters, suppressed the renal proinflammatory marker, NF-kappa B, abrogated the elevated renal hydroxyprolin, and decreased the enhanced renal nicotinamide adenine dinucleotide phosphate oxidase activity with parallel reduction of urinary oxidative stress markers. On the contrary, treatment with ZnPP abrogated HO-1 levels, aggravated the diabetic condition with further increases in renal oxidative stress, fibrotic and inflammatory markers, and exacerbated renal dysfunction in diabetic animals. These findings suggest that the reduced diabetic renal injury upon HO-1 induction implicates the role of HO-1 induction as a potential treatment for DN.
引用
收藏
页码：413 / 427
页数：15
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