中国组织工程研究与临床康复2011，Vol.15Issue(53)：10007-10010,4.DOI:10.3969/j.issn.1673-8225.2011.53.031
鼻饲热休克蛋白65诱导免疫耐受降低动脉粥样硬化的形成及其机制
Effect of nasal tolerance induction to heat shock protein-65 on atherosclerosis and potential mechanism
摘要
Abstract
BACKGROUND: A body of evidences support that CD4*CD25*Foxp3* regulatory T cells is associated wrth oral toleranceinduction and inhibition of atherosclerosis, but little is described whether nasal tolerance to antigen Ikewise induce the regulatoryT cell production and antiatherosclerotic benefit.OBJECTIVE: To investigate the effect of nasal tolerance induction to heat shock protein-65(HSP65) on atherogenesis andpotential mechanism.METHODS: Six-week-old male ApoE^" mice were nasalry administrated HSP65 or phosphate buffer as control. Cryo-section wasused to examine 1he size of atheromatous plaque area of aortic root in ApeE* mice with sbdeen-week-old; fluorescence actn/atedcell sorter was used to analyse the production level of CD4*CD25*Fo*p3* regulatory T cells; ELISA was applied to determine thelevel of cytokines transforming growth factor beta (TOF-6).RESULT SANO CONCLUSION: Eight weeks after nasal administration, the results of cryo-section showed that H S PCS-teatedmice had a marked decrease by 32.7% in ath er om atous plaque area of aortic root as compared with the control group (F<O01).At 14da^s after the last nasal treatment the percentage of CD4*CD25*Foxp3* regulatory T celt in total CD4* T cells from treatedmice increased significant^ as compared with the control group (f < 0.01). at 4.14 days and 8 weeks after the last nasaladministration, cytokine TOF-6 level from nasal HSP65 mice increased remarkabry compared with the control group on the abovethree points. So. nasal tolerance induction to heat shock protein-65 inhibits atherosclerotic formation by inducinga nti-inflammatory cytokine T<?F-l5-dependent regulatory T celts. It is proposed that nasal tolerance induction to HSP6S mayprovide an afternatru-e therapeutic method to atherosclerosis.关键词
动脉粥样硬化/免疫耐受/热休克蛋白/调节性T细胞/鼻饲分类
医药卫生引用本文复制引用
李海禹,丁艳萍,曾秋棠..鼻饲热休克蛋白65诱导免疫耐受降低动脉粥样硬化的形成及其机制[J].中国组织工程研究与临床康复,2011,15(53):10007-10010,4.基金项目
国家自然基金项目一部分(81070237),课题名称:经鼻诱导Th3细胞活化负向调节动脉粥样硬化机制研究. （81070237）
