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Article: More severe type 2 diabetes-associated ischemic stroke injury is alleviated in aldose reductase-deficient mice

TitleMore severe type 2 diabetes-associated ischemic stroke injury is alleviated in aldose reductase-deficient mice
Authors
KeywordsAnimal model
Db/db mouse
Ischemia
Reperfusion
Retina
Issue Date2010
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828
Citation
Journal Of Neuroscience Research, 2010, v. 88 n. 9, p. 2026-2034 How to Cite?
AbstractAldose reductase (AR), the first enzyme in the polyol pathway, has been implicated in a wide variety of physiological and pathological functions, such as diabetic vascular and neural complications. It is known that diabetes mellitus can exacerbate brain and retina damage after ischemic injuries. However, the underlying mechanisms are not clear. In the present study, we made use of db/db mice with an AR null mutation (AR-/-db/db) to understand better the role of AR in the pathogenesis of brain and retina ischemic injuries under diabetic conditions. Cerebral and retinal ischemia was induced by transient middle cerebral artery occlusion in control and diabetic mice either with or without an AR null mutation. Mice were evaluated for neurological deficits after 30 min of ischemia and 23.5 hr of reperfusion. Our results showed that the diabetic db/db mice had significantly more severe neurological deficit and larger brain infarct size than the nondiabetic mice. Compared with wild-type db/db mice, the AR-/-db/db mice had significantly lower neurological scores, smaller brain infarct areas, and less hemispheric brain swelling. Retinal swelling was also significantly decreased in the AR -/-db/db mice. Less swelling in the brain and retina of the AR -/-db/db mice correlated with less expression of the water channel aquaporin 4. Taken together, these data clearly show that deletion of AR leads to less severe brain and retinal ischemic injuries in the diabetic db/db mouse. The present study indicates that inhibition of AR in diabetics may protect against damage in the brain and retina following ischemic reperfusion injury. © 2010 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/127690
ISSN
2015 Impact Factor: 2.689
2015 SCImago Journal Rankings: 1.261
ISI Accession Number ID
Funding AgencyGrant Number
GRFHKU 7313
University Development Fund
Funding Information:

Contract grant sponsor: GRF; Contract grant number: HKU 7313 (to S.K.C.); Contract grant sponsor: University Development Fund.

References

 

DC FieldValueLanguage
dc.contributor.authorYeung, CMen_HK
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorCheung, AKHen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorWong, Den_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-10-31T13:40:21Z-
dc.date.available2010-10-31T13:40:21Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Neuroscience Research, 2010, v. 88 n. 9, p. 2026-2034en_HK
dc.identifier.issn0360-4012en_HK
dc.identifier.urihttp://hdl.handle.net/10722/127690-
dc.description.abstractAldose reductase (AR), the first enzyme in the polyol pathway, has been implicated in a wide variety of physiological and pathological functions, such as diabetic vascular and neural complications. It is known that diabetes mellitus can exacerbate brain and retina damage after ischemic injuries. However, the underlying mechanisms are not clear. In the present study, we made use of db/db mice with an AR null mutation (AR-/-db/db) to understand better the role of AR in the pathogenesis of brain and retina ischemic injuries under diabetic conditions. Cerebral and retinal ischemia was induced by transient middle cerebral artery occlusion in control and diabetic mice either with or without an AR null mutation. Mice were evaluated for neurological deficits after 30 min of ischemia and 23.5 hr of reperfusion. Our results showed that the diabetic db/db mice had significantly more severe neurological deficit and larger brain infarct size than the nondiabetic mice. Compared with wild-type db/db mice, the AR-/-db/db mice had significantly lower neurological scores, smaller brain infarct areas, and less hemispheric brain swelling. Retinal swelling was also significantly decreased in the AR -/-db/db mice. Less swelling in the brain and retina of the AR -/-db/db mice correlated with less expression of the water channel aquaporin 4. Taken together, these data clearly show that deletion of AR leads to less severe brain and retinal ischemic injuries in the diabetic db/db mouse. The present study indicates that inhibition of AR in diabetics may protect against damage in the brain and retina following ischemic reperfusion injury. © 2010 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828en_HK
dc.relation.ispartofJournal of Neuroscience Researchen_HK
dc.rightsJournal of Neuroscience Research. Copyright © John Wiley & Sons, Inc.-
dc.subjectAnimal modelen_HK
dc.subjectDb/db mouseen_HK
dc.subjectIschemiaen_HK
dc.subjectReperfusionen_HK
dc.subjectRetinaen_HK
dc.subject.meshAldehyde Reductase - deficiency - genetics - metabolism-
dc.subject.meshBrain Ischemia - enzymology - metabolism - pathology-
dc.subject.meshDiabetes Mellitus, Type 2 - complications - enzymology - metabolism - pathology-
dc.subject.meshRetinal Diseases - enzymology - metabolism - pathology-
dc.subject.meshStroke - enzymology - metabolism - pathology-
dc.titleMore severe type 2 diabetes-associated ischemic stroke injury is alleviated in aldose reductase-deficient miceen_HK
dc.typeArticleen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailWong, D: shdwong@hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityWong, D=rp00516en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jnr.22349en_HK
dc.identifier.pmid20143423-
dc.identifier.scopuseid_2-s2.0-77953481998en_HK
dc.identifier.hkuros182901en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953481998&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume88en_HK
dc.identifier.issue9en_HK
dc.identifier.spage2026en_HK
dc.identifier.epage2034en_HK
dc.identifier.isiWOS:000278056600020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYeung, CM=7201354151en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.scopusauthoridCheung, AKH=7401806412en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridWong, D=7401536078en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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