• Osaze Edosuyi, Myung Choi, Vashti Edosuyi, Ighodaro Igbe, and Adebayo Oyekan.
• Bratisl Med J. 2023 Jan 1; 124 (2): 151157151-157.

BackgroundMalate, the tricarboxylic acid (TCA) cycle intermediary, upregulates renal nitric oxide (NO) signaling, and NO is renoprotective in nephropathy.ObjectivesThis study explored the hypothesis that malate could increase renal NO and decrease renal injury and fibrotic markers in obstructive nephropathy.MethodsKidney 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.ResultsMalate 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.ConclusionMalate ameliorated the injury and inflammation but selectively reduced fibrosis in obstructive nephropathy (Fig. 6, Ref. 32). Text in PDF www.elis.sk Keywords: Malate, tricarboxylic acid cycle, nitric oxide, kidney injury molecule (KIM-1), obstructive nephropathy.

21 keywords...

hide…