Sodium thiosulfate treatment rescues hyperglycaemia-induced pronephros damage in zebrafish by upregulating nitric oxide signalling

被引:0
|
作者
Ott, Hannes [1 ]
Bennewitz, Katrin [1 ]
Zhang, Xin [1 ]
Prianichnikova, Mariia [1 ]
Sticht, Carsten [2 ]
Poschet, Gernot [3 ]
Kroll, Jens [1 ]
机构
[1] Heidelberg Univ, Med Fac Mannheim, European Ctr Angioscience ECAS, Dept Vasc Biol & Tumor Angiogenesis, Mannheim, Germany
[2] Heidelberg Univ, Med Fac Mannheim, NGS Core Facil, Mannheim, Germany
[3] Heidelberg Univ, Ctr Organismal Studies, Metabol Core Technol Platform, Heidelberg, Germany
关键词
diabetes mellitus; nitric oxide; sodium thiosulfate; zebrafish; HYDROGEN-SULFIDE; DIABETIC-NEPHROPATHY; INDUCED HYPERTENSION; RAT HEARTS; PROTECTS; INJURY; KIDNEY; ANGIOGENESIS; PROTEINURIA; METABOLITE;
D O I
10.1113/JP286398
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
figure legend Sodium thiosulfate (STS) rescues the pronephros phenotype of pdx1 morphants through compensatory upregulation of nitric oxide (NO) metabolism. Zebrafish larvae injected with a control morpholino show the typical pronephros structure at 48 h post-fertilization (hpf) with and without STS treatment. In pdx1 morphants, citrulline concentration is decreased and arginine and proline metabolism show reduced activity, indicating downregulated NO metabolism and leading to pronephros damage at 48 hpf. Treatment with STS resulted in higher arginine and citrulline concentrations, implying an increased production of NO, leading to the rescue of the pronephros of pdx1 morphants at 48 hpf. image
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页数:14
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