| Interleukin-2 protects against endothelial dysfunction induced by high glucose levels in rats. | |
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MedLine Citation:
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PMID: 16837248 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS: Interleukin-2 (IL-2) can modulate cardiovascular functions, but the effect of IL-2 on vascular endothelial function in diabetes is not known. We hypothesized that IL-2 may attenuate endothelial dysfunction induced by high glucose or diabetes. So the aim of this study was to investigate the effect of IL-2 on endothelium-response of aortas incubated with high glucose or from diabetic rats and its underlying mechanism. METHODS: Acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR), sodium nitroprusside (SNP)-induced endothelium-independent relaxation (EIR), superoxide dismutase (SOD) and nitric oxide synthase (NOS) were measured in aortas isolated from non-diabetic rats and exposed to a high glucose concentration and from streptozotocin-induced diabetic rats. RESULTS: Incubation of aortic rings with high glucose (44 mM) for 4 h resulted in a significant inhibition of EDR, but had no effects on EIR. Co-incubation with IL-2 for 40 min prevented the inhibition of EDR caused by high glucose in a concentration-dependent manner. Similarly, high glucose decreased SOD and NOS activity in aortic tissue. IL-2 (1000 U/ml) significantly attenuated the decrease of SOD and NOS activity caused by high glucose. In addition, EDR declined along with the decrease of serum NO level in aortas from STZ-induced diabetic rats. Injection of IL-2 (5000 and 50,000 U kg(-1) d(-1), s.c.) for 5 weeks prevented the inhibition of EDR and the decrease of serum NO levels caused by diabetes. CONCLUSIONS: IL-2 significantly ameliorated the endothelial dysfunction induced by hyperglycemia, in which the activation of the NO pathway and SOD may be involved. |
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Authors:
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Ling-Bo Qian; Hui-Ping Wang; Wei-Ling Qiu; He Huang; Iain C Bruce; Qiang Xia |
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Publication Detail:
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Type: In Vitro; Journal Article Date: 2006-06-12 |
Journal Detail:
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Title: Vascular pharmacology Volume: 45 ISSN: 1537-1891 ISO Abbreviation: Vascul. Pharmacol. Publication Date: 2006 Dec |
Date Detail:
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Created Date: 2006-11-24 Completed Date: 2007-02-15 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101130615 Medline TA: Vascul Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 374-82 Citation Subset: IM |
Affiliation:
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Department of Physiology, Zhejiang University School of Medicine, 353 Yan-an Road, Hangzhou 310031, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Animals Aorta, Thoracic / drug effects*, metabolism, physiopathology Diabetes Mellitus, Experimental / blood, physiopathology* Dose-Response Relationship, Drug Endothelium, Vascular / drug effects*, metabolism, physiopathology Glucose / pharmacology* Interleukin-2 / pharmacology* Male Nitric Oxide / blood Nitric Oxide Synthase / metabolism Nitroprusside / pharmacology Rats Rats, Sprague-Dawley Superoxide Dismutase / metabolism Time Factors Vasodilation / drug effects* Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-2; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 50-99-7/Glucose; 51-84-3/Acetylcholine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.15.1.1/Superoxide Dismutase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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