Chronic NaHS treatment decreases oxidative stress and improves endothelial function in diabetic mice

Hydrogen sulphide (H2S) is endogenously produced in vascular tissue and has anti-oxidant and vasoprotective properties. This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with st...

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Published in:Diabetes & vascular disease research 2017-05, Vol.14 (3), p.246-253
Main Authors: Ng, Hooi H, Yildiz, Gunes S, Ku, Jacqueline M, Miller, Alyson A, Woodman, Owen L, Hart, Joanne L
Format: Article
Language:English
Subjects:
Animals
Antioxidants - administration & dosage
Blood Glucose - metabolism
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - drug therapy
Diabetic Angiopathies - etiology
Diabetic Angiopathies - metabolism
Diabetic Angiopathies - physiopathology
Diabetic Angiopathies - prevention & control
Dose-Response Relationship, Drug
Drug Administration Schedule
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Glycated Hemoglobin A - metabolism
Male
Mice, Inbred C57BL
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - physiopathology
NADPH Oxidase 2 - metabolism
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitric Oxide Synthase Type III - metabolism
Oxidative Stress - drug effects
Sulfides - administration & dosage
Superoxides - metabolism
Time Factors
Vasodilation - drug effects
Vasodilator Agents - pharmacology
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container_end_page 253
container_issue 3
container_start_page 246
container_title Diabetes & vascular disease research
container_volume 14
creator Ng, Hooi H
Yildiz, Gunes S
Ku, Jacqueline M
Miller, Alyson A
Woodman, Owen L
Hart, Joanne L
description Hydrogen sulphide (H2S) is endogenously produced in vascular tissue and has anti-oxidant and vasoprotective properties. This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with streptozotocin (60 mg/kg daily, ip for 2 weeks) and confirmed by elevated blood glucose and glycated haemoglobin levels. Diabetic mice were then treated with NaHS (100 µmol/kg/day) for 4 weeks, and aortae collected for functional and biochemical analyses. In the diabetic group, both endothelium-dependent vasorelaxation and basal nitric oxide (NO•) bioactivity were significantly reduced (p 
doi_str_mv 10.1177/1479164117692766
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This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with streptozotocin (60 mg/kg daily, ip for 2 weeks) and confirmed by elevated blood glucose and glycated haemoglobin levels. Diabetic mice were then treated with NaHS (100 µmol/kg/day) for 4 weeks, and aortae collected for functional and biochemical analyses. In the diabetic group, both endothelium-dependent vasorelaxation and basal nitric oxide (NO•) bioactivity were significantly reduced (p &lt; 0.05), and maximal vasorelaxation to the NO• donor sodium nitroprusside was impaired (p &lt; 0.05) in aorta compared to control mice. Vascular superoxide generation via nicotine adenine dinucleotide phosphate (NADPH) oxidase (p &lt; 0.05) was elevated in aorta from diabetic mice which was associated with increased expression of NOX2 (p &lt; 0.05). NaHS treatment of diabetic mice restored endothelial function and exogenous NO• efficacy back to control levels. NaHS treatment also reduced the diabetes-induced increase in NADPH oxidase activity, but did not affect NOX2 protein expression. 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This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with streptozotocin (60 mg/kg daily, ip for 2 weeks) and confirmed by elevated blood glucose and glycated haemoglobin levels. Diabetic mice were then treated with NaHS (100 µmol/kg/day) for 4 weeks, and aortae collected for functional and biochemical analyses. In the diabetic group, both endothelium-dependent vasorelaxation and basal nitric oxide (NO•) bioactivity were significantly reduced (p &lt; 0.05), and maximal vasorelaxation to the NO• donor sodium nitroprusside was impaired (p &lt; 0.05) in aorta compared to control mice. Vascular superoxide generation via nicotine adenine dinucleotide phosphate (NADPH) oxidase (p &lt; 0.05) was elevated in aorta from diabetic mice which was associated with increased expression of NOX2 (p &lt; 0.05). NaHS treatment of diabetic mice restored endothelial function and exogenous NO• efficacy back to control levels. NaHS treatment also reduced the diabetes-induced increase in NADPH oxidase activity, but did not affect NOX2 protein expression. 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dosage</topic><topic>Superoxides - metabolism</topic><topic>Time Factors</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ng, Hooi H</creatorcontrib><creatorcontrib>Yildiz, Gunes S</creatorcontrib><creatorcontrib>Ku, Jacqueline M</creatorcontrib><creatorcontrib>Miller, Alyson A</creatorcontrib><creatorcontrib>Woodman, Owen L</creatorcontrib><creatorcontrib>Hart, Joanne L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes &amp; vascular disease research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Ng, Hooi H</au><au>Yildiz, Gunes S</au><au>Ku, Jacqueline M</au><au>Miller, Alyson A</au><au>Woodman, Owen L</au><au>Hart, Joanne L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic NaHS treatment decreases oxidative stress and improves endothelial function in diabetic mice</atitle><jtitle>Diabetes &amp; 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This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with streptozotocin (60 mg/kg daily, ip for 2 weeks) and confirmed by elevated blood glucose and glycated haemoglobin levels. Diabetic mice were then treated with NaHS (100 µmol/kg/day) for 4 weeks, and aortae collected for functional and biochemical analyses. In the diabetic group, both endothelium-dependent vasorelaxation and basal nitric oxide (NO•) bioactivity were significantly reduced (p &lt; 0.05), and maximal vasorelaxation to the NO• donor sodium nitroprusside was impaired (p &lt; 0.05) in aorta compared to control mice. Vascular superoxide generation via nicotine adenine dinucleotide phosphate (NADPH) oxidase (p &lt; 0.05) was elevated in aorta from diabetic mice which was associated with increased expression of NOX2 (p &lt; 0.05). NaHS treatment of diabetic mice restored endothelial function and exogenous NO• efficacy back to control levels. NaHS treatment also reduced the diabetes-induced increase in NADPH oxidase activity, but did not affect NOX2 protein expression. These data show that chronic NaHS treatment reverses diabetes-induced vascular dysfunction by restoring NO• efficacy and reducing superoxide production in the mouse aorta.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>28467198</pmid><doi>10.1177/1479164117692766</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Antioxidants - administration & dosage
Blood Glucose - metabolism
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - drug therapy
Diabetic Angiopathies - etiology
Diabetic Angiopathies - metabolism
Diabetic Angiopathies - physiopathology
Diabetic Angiopathies - prevention & control
Dose-Response Relationship, Drug
Drug Administration Schedule
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Glycated Hemoglobin A - metabolism
Male
Mice, Inbred C57BL
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - physiopathology
NADPH Oxidase 2 - metabolism
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitric Oxide Synthase Type III - metabolism
Oxidative Stress - drug effects
Sulfides - administration & dosage
Superoxides - metabolism
Time Factors
Vasodilation - drug effects
Vasodilator Agents - pharmacology
title Chronic NaHS treatment decreases oxidative stress and improves endothelial function in diabetic mice
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