Publication:
Effect of a hypercholesterolemia as a starting factor on spinal degeneration in rabbits and role of vitamin E (α-tocopherol)

dc.contributor.coauthorAydın A. L.
dc.contributor.coauthorAytan, N.
dc.contributor.coauthorYapıcıer, O.
dc.contributor.coauthorÖktenoğlu T. ,Özer, N. K.
dc.contributor.departmentN/A
dc.contributor.kuauthorSasani, Mehdi
dc.contributor.kuauthorÖzer, Ali Fahir
dc.contributor.kuprofileFaculty Member
dc.contributor.kuprofileFaculty Member
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.contributor.yokidN/A
dc.contributor.yokid1022
dc.date.accessioned2024-11-09T12:44:56Z
dc.date.issued2016
dc.description.abstractBackground: To identify the role of the hypercholesterolemia as a starting factor in discovertebral degeneration that ultimately causes lower back pain, and investigate the role of Vitamin E in this process. Methods: The rabbits (n = 32) were divided into two broad experimental groups: A control group, and a hypercholesterolemia group, namely cholesterol, and cholesterol plus Vitamin E groups and they were fed sequentially for 4 or 8 weeks. Serum cholesterol and Vitamin E (a-tocopherol) levels were determined; vascular tissue was prepared for histopathological analyses and vertebra was decalcifed for the study. Results: Cholesterol diet group resulted approximately 44-fold of increase plasma cholesterol levels over the 4-week control values. Additional supplementation with Vitamin E group induced a plasma cholesterol level increase of only 37-fold as compared to the control group. In the cholesterol groups, light microscope examination revealed atherosclerotic plaque in major arteries. However, in the cholesterol plus Vitamin E treatment groups, no lipid accumulation or foam cell formation was visible in the abdominal aorta and vertebral segmental artery. In histopathological examination, we found degenerative changes in the discovertebral unit in cholesterol treated groups. Conclusion: Hypercholesterolemia causes fat accumulation in the disc endplate and vertebral body that causes blood supply disturbances which might be a starting factor of discovertebral degeneration. This event was not reversed by the elimination of cholesterol from the diet. Vitamin E supplementation was not effective in reducing fat accumulation in vertebral bone marrow. As a result, we conclude that degeneration of the discovertebral unit is not related to atherosclerotic changes in the major blood vessels. © 2016 Surgical Neurology International | Published by Wolters Kluwer-Medknow.
dc.description.fulltextYES
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue36
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipN/A
dc.description.versionPublisher version
dc.description.volume7
dc.formatpdf
dc.identifier.doi10.4103/2152-7806.180092
dc.identifier.eissn2152-7806
dc.identifier.embargoNO
dc.identifier.filenameinventorynoIR00870
dc.identifier.issn2152-7806
dc.identifier.linkhttps://doi.org/10.4103/2152-7806.180092
dc.identifier.quartileN/A
dc.identifier.scopus2-s2.0-85007124597
dc.identifier.urihttps://hdl.handle.net/20.500.14288/2421
dc.keywordsHypercholesteremia
dc.keywordsBackache
dc.keywordsVitamin E
dc.keywordsPhysiological effects of cholesterol
dc.keywordsLipid analysis
dc.keywordsCase studies
dc.keywordsAtherosclerosis
dc.keywordsDisc degeneration
dc.keywordsHypercholesterolemia
dc.keywordsRabbit spine
dc.keywordsSpine degenerative disease
dc.keywordsVitamin E
dc.languageEnglish
dc.publisherMedknow Publications
dc.relation.urihttp://cdm21054.contentdm.oclc.org/cdm/ref/collection/IR/id/868
dc.sourceSurgical Neurology International
dc.subjectMedicine
dc.subjectNeurosurgery
dc.titleEffect of a hypercholesterolemia as a starting factor on spinal degeneration in rabbits and role of vitamin E (α-tocopherol)
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authoridN/A
local.contributor.authorid0000-0001-7285-381X
local.contributor.kuauthorSasani, Mehdi
local.contributor.kuauthorÖzer, Ali Fahir

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