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The Effect Of Inhibition Of Galectin-3 Expression On Intimal Hyperplasia In Rats After Carotid Artery Balloon Injury And Its Mechanism Rats

Posted on:2018-08-04Degree:MasterType:Thesis
Country:ChinaCandidate:Y H TanFull Text:PDF
GTID:2334330542471491Subject:Clinical Medicine
Abstract/Summary:PDF Full Text Request
Objective:By constructing a rat carotid artery injury model while giving Galectin-3 inhibitor modified citrus pectin(MCP)process,observe the lesion intimal hyperplasia,and and explore the role of galectin-3 in intimal hyperplasia in vascular injury and the effect of MCP on that.Methods:Ninety male Wistar rats,10-week-old,were randomly divided into sham operation group,operation group and treatment group,with 30 rats in each group.Both operation group and treatment group were treated with left carotid artery balloon injury,1 week before which,operation group and the treeatment group were intervented with normal saline and 10%MCP daily,respectively,till sacrificed for sample collection.sham operation group intervented with normal saline in the same manner as operation group did was treated with left carotid artery dissection.After the treatment discribed above,blood sample was collected via tail vein immediately,while heart blood and left carotid artery were collected on 7d,14 d and 28 d after operation respectively.ELISA were used to detected serum level of Gal-3,TNF-alpha and VEGF;the changes of vascular lumen and intimal hyperplasia were observed by HE staining;the expression Gal-3,VCAM-1 and ICAM-1 were detected by western blot analysis.Results:1.serological results detected by ELISA: The experssion of Gal-3,TNF-alpha and VEGF were observed in each group,no significant difference were detected in the expression of those protein at different interval in sham operation group;seven days after operation,the maximum increase of those protein were observed in both operation group and treatment group.Compared with sham operation group,the serum expression of Gal-3,TNF-and VEGF in both operation group and treatment group were significantly increased(P<0.05),but which was significantly decreased in treatment group compared with operation group(P<0.05).2.HE staining and morphology observation by light microscope: seven days after operation,intimal denudation rather than obvious neointima formation was detected in balloon injuried vascular in both operation group and treatment group compared with sham operation group;on the 14 day and 28 day postoperation,the vessel in sham operation group was characterize by smooth intimal membrane,media mainly consisted of smooth muscle cells without collagen deposition and adventitia formed by connective tissue.Obvious morphology change in the vessel were detected in both operation group and treatment group,which is characterized by remark intimal membrane hyperplasia,disorderly arrangement of smooth muscle cells in media,infiltration of macrophages,increased extracellular matrix,collagen deposition,increased intima / media ratio and smaller vascular lumen compared with sham operation group.Compared with the operation group,the intima hyperplasia,wall thickness and lumen stenosis of treatment group were significantly reduced.3.Western blot analysis: The experssion of Gal-3,VCAM-1 and ICAM-1 in vascular tissues were low at different interval in sham operation group,while the expression of those protein were significantly increased in both operation group and treatment group.Compared with operation group,the expression of those protein was remarkly decreased in treatment group(P<0.05).Conclusions:The results idicated that Galectin-3 had an inducative effect on intimal hyperplasia and restenosis by mediating adhesion between vascular endothelial cells and inflammatory cells to promote inflammatory.specific Galectin-3 inhibitor MCP can inhibit occurence and development of intimal hyperplasia and stenosis.Galectin-3 may be a new target for the prevention and treatment of intimal hyperplasia and stenosis in carotid artery.
Keywords/Search Tags:Galectin-3, modified citrus pectin, tumor necrosis factor alpha, vascular endothelial growth factor, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, intimal hyperplasia
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