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Article: Allopurinol attenuates left ventricular dysfunction in rats with early stages of streptozotocin-induced diabetes

TitleAllopurinol attenuates left ventricular dysfunction in rats with early stages of streptozotocin-induced diabetes
Authors
Issue Date2012
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394
Citation
Diabetes - Metabolism: Research and Reviews, 2012, v. 28 n. 5, p. 409-417 How to Cite?
Abstract
BACKGROUND: Xanthine oxidase-derived superoxide production and oxidative stress contribute to the development of diabetic complications including diabetic cardiomyopathy. We hypothesized that xanthine oxidase-inhibitor allopurinol (ALP) may decrease hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis, and attenuate the development of left ventricle (LV) diastolic dysfunction in rats with streptozotocin (STZ)-induced diabetes. METHODS: Control Sprague Dawley (C) or streptozotocin-induced diabetic (D) rats were either untreated or treated with allopurinol (100 mg/kg/day) for 4 weeks starting at 1 week after streptozotocin injection. Free 15-F2t-isoprostane, a specific indicator of oxidative stress was measured by enzymatic immunoassay. The cardiomyocyte cross-sectional area was assessed by hematoxylin and eosin-stained paraffin-embedded sections of LVs. Myocardial collagens I and III were assessed by immunol histochemistry and Western blotting. Echocardiography was performed to characterize cardiac structure and function. RESULTS: In diabetic rats, both plasma and cardiac tissue levels of free 15-F2t-isoprostane were increased (p < 0.05 vs. control), accompanied with significant increase (p < 0.05 vs. control) in cross-section area and myocardial collagen deposition of LV cardiomyocyte. Echocardiography in diabetic rats showed that LV weight/body weight ratio was significantly higher than in control rats, whereas the levels of LV end-diastolic volume and stroke volume were decreased (all p < 0.05 diabetic vs. control). All these changes were either attenuated or prevented by allopurinol. In addition, LV ejection fraction in diabetic rats treated with allopurinol was higher than that in untreated diabetic rats (p < 0.05). CONCLUSION: Allopurinol can attenuate hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis and subsequently prevent left ventricular dysfunction in early diabetes. Copyright (c) 2012 John Wiley and Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/159256
ISSN
ISI Accession Number ID

 

Author Affiliations
  1. The University of Hong Kong
  2. Shenzhen Futian District Traditional Chinese Medicine Hospital
  3. Capital Medical University China
DC FieldValueLanguage
dc.contributor.authorGao, Xen_US
dc.contributor.authorXu, Yen_US
dc.contributor.authorXu, Ben_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorCai, Jen_US
dc.contributor.authorLiu, HMen_US
dc.contributor.authorLei, Sen_US
dc.contributor.authorZhong, YQen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-08-16T05:47:13Z-
dc.date.available2012-08-16T05:47:13Z-
dc.date.issued2012en_US
dc.identifier.citationDiabetes - Metabolism: Research and Reviews, 2012, v. 28 n. 5, p. 409-417en_US
dc.identifier.issn1520-7552-
dc.identifier.urihttp://hdl.handle.net/10722/159256-
dc.description.abstractBACKGROUND: Xanthine oxidase-derived superoxide production and oxidative stress contribute to the development of diabetic complications including diabetic cardiomyopathy. We hypothesized that xanthine oxidase-inhibitor allopurinol (ALP) may decrease hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis, and attenuate the development of left ventricle (LV) diastolic dysfunction in rats with streptozotocin (STZ)-induced diabetes. METHODS: Control Sprague Dawley (C) or streptozotocin-induced diabetic (D) rats were either untreated or treated with allopurinol (100 mg/kg/day) for 4 weeks starting at 1 week after streptozotocin injection. Free 15-F2t-isoprostane, a specific indicator of oxidative stress was measured by enzymatic immunoassay. The cardiomyocyte cross-sectional area was assessed by hematoxylin and eosin-stained paraffin-embedded sections of LVs. Myocardial collagens I and III were assessed by immunol histochemistry and Western blotting. Echocardiography was performed to characterize cardiac structure and function. RESULTS: In diabetic rats, both plasma and cardiac tissue levels of free 15-F2t-isoprostane were increased (p < 0.05 vs. control), accompanied with significant increase (p < 0.05 vs. control) in cross-section area and myocardial collagen deposition of LV cardiomyocyte. Echocardiography in diabetic rats showed that LV weight/body weight ratio was significantly higher than in control rats, whereas the levels of LV end-diastolic volume and stroke volume were decreased (all p < 0.05 diabetic vs. control). All these changes were either attenuated or prevented by allopurinol. In addition, LV ejection fraction in diabetic rats treated with allopurinol was higher than that in untreated diabetic rats (p < 0.05). CONCLUSION: Allopurinol can attenuate hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis and subsequently prevent left ventricular dysfunction in early diabetes. Copyright (c) 2012 John Wiley and Sons, Ltd.-
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394-
dc.relation.ispartofDiabetes - Metabolism: Research and Reviewsen_US
dc.rightsDiabetes - Metabolism: Research and Reviews. Copyright © John Wiley & Sons Ltd.-
dc.titleAllopurinol attenuates left ventricular dysfunction in rats with early stages of streptozotocin-induced diabetesen_US
dc.typeArticleen_US
dc.identifier.emailGao, X: elngao@163.comen_US
dc.identifier.emailLiu, HM: huimin_liu2006@126.comen_US
dc.identifier.emailLei, S: shqlei@hku.hken_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hk-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.doi10.1002/dmrr.2295-
dc.identifier.pmid22389139-
dc.identifier.scopuseid_2-s2.0-84863773463-
dc.identifier.hkuros204903en_US
dc.identifier.hkuros203048-
dc.identifier.volume28en_US
dc.identifier.issue5en_US
dc.identifier.spage409en_US
dc.identifier.epage417en_US
dc.identifier.isiWOS:000306127400005-
dc.publisher.placeUnited Kingdom-

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