期刊论文详细信息
Bratislava Medical Journal
Malate reduced kidney injury molecule (KIM-1) expression and selectively upregulated the renal nitric oxide production in obstructive nephropathy
article
Osaze EDOSUYI1  Myung CHOI2  Vashti EDOSUYI3  Ighodaro IGBE1  Adebayo OYEKAN2 
[1] Department of Pharmacology & Toxicology, Faculty of Pharmacy, University of Benin;Center for Cardiovascular Diseases, Gray Hall Suites College of Pharmacy & Health Sciences Texas Southern University;Department of Child Health, University of Benin Teaching Hospital
关键词: Malate;    tricarboxylic acid cycle;    nitric oxide;    kidney injury molecule (KIM-1);    obstructive nephropathy;   
DOI  :  10.4149/BLL_2023_024
学科分类:医学(综合)
来源: AEPress, s.r.o.
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【 摘 要 】

BACKGROUND: Malate, the tricarboxylic acid (TCA) cycle intermediary, upregulates renal nitric oxide (NO) signaling, and NO is renoprotective in nephropathy. OBJECTIVES: This study explored the hypothesis that malate could increase renal NO and decrease renal injury and fibrotic markers in obstructive nephropathy. METHODS: Kidney injury was induced in rats via unilateral surgical ligation of the ureter, there after, rats were treated with malate (600 mg/kg, p.o.) for ten days. Urine was collected on days 0, 4, 7 and 10. Urinary sodium excretion was also determined. Western blot and biochemical analyses were carried on the nephropathic kidneys. RESULTS: Malate reduced kidney injury molecule (KIM-1) expression in the renal cortex and medulla of nephropathic rats (p < 0.05). NO production was selectively increased in the medulla of nephropathic rats treated with malate (58.3 ± 1.3 vs 77.8 ± 4.4 µM/ng, p < 0.05). Superoxide dismutase and catalase activity increased in the kidney of malate-treated nephropathic rats (p < 0.05). Transforming growth factor (TGF-β), an index of fibrosis, increased in the cortex but not medulla of the malate-treated UUO group. There was a consistent increase in collagenase activity in the cortex, and a reduction in the medulla. CONCLUSION: Malate ameliorated the injury and inflammation but selectively reduced fibrosis in obstructive nephropathy (Fig. 6, Ref. 32).

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