当前位置:主页 > 医学论文 > 急救学论文 >

经静脉移植骨髓基质干细胞对急性心肌梗死Toll样受体4蛋白表达的影响

发布时间:2018-07-05 03:49

  本文选题:急性心肌梗死 + 骨髓基质干细胞 ; 参考:《大连医科大学》2013年硕士论文


【摘要】:目的:探讨经静脉移植自体骨髓基质干细胞治疗急性心肌梗死对新西兰兔心肌组织细胞Toll样受体4蛋白(Toll like receptor4,TLR4)表达情况的影响。 方法:将60只健康新西兰兔随机分为假手术组、手术组及治疗组3组,每组20只。手术组及治疗组新西兰兔顺次开胸,结扎左冠状动脉前降支中部1/2处建立急性心肌梗死动物模型,,假手术组开胸于相同部位穿入手术缝线,但不结扎。制膜后第2周,治疗组经耳缘静脉植入自体骨髓基质干细胞,手术组及假手术组植入与骨髓基质干细胞相等量的磷酸缓冲液(PBS);移植4周后分别取出各组心脏,通过蛋白免疫印迹技术(Western-blotting)检测三组心肌组织中TLR4表达的情况。通过Gel-Pro Analyzer软件测定蛋白条带灰度值,计算TLR4的相对定量。组间比较采用秩和检验,数据采用中位数、百分位数(上四分位数,下四分位数)表示,以P0.05为差异有统计学意义。 结果:手术组缺血坏死心肌组织内的TLR4表达明显高于假手术组(P<0.05),治疗组心肌组织内的TLR4的表达低于手术组(P<0.05),但高于假手术组(P<0.05)。 结论:1.急性心肌梗死发生后TLR4的表达迅速上调,提示TLR4在急性心肌梗死的发病过程中具有重要的意义,其可能作为重要的炎性受体介导心肌组织的缺血炎性损伤;2.自体骨髓基质干细胞移植于发生急性心肌梗死的心肌组织后可以生存、分化;3.经耳缘静脉移植自体骨髓基质干细胞可以治疗急性心肌梗死,其机制之一可能与抑制TLR4所介导的炎性反应有关,其可在一定程度上抑制参与TLR4介导的炎症反应的炎性因子的合成及释放。
[Abstract]:Aim: to investigate the effect of intravenous transplantation of autologous bone marrow stromal cells (BMSCs) on the expression of Toll like receptor 4 (TLR4) in myocardial tissue of New Zealand rabbits. Methods: 60 healthy New Zealand rabbits were randomly divided into sham operation group, operation group and treatment group with 20 rabbits in each group. New Zealand rabbits in operation group and treatment group were treated with thoracotomy sequentially, and acute myocardial infarction model was established by ligating left anterior descending coronary artery at 1 / 2 of the middle of left coronary artery. In sham-operation group, the thoracotomy was perforated into the suture of operation at the same position, but not ligated. At the second week after membrane preparation, autologous bone marrow stromal stem cells were implanted through the auricular vein in the treatment group, and PBS was implanted in the operation group and the sham operation group in the same amount as the bone marrow stromal stem cells. The hearts of each group were removed after 4 weeks of transplantation. The expression of TLR4 was detected by Western blotting. The relative quantification of TLR4 was calculated by Gel-Pro Analyzer software. The data were expressed as median, percentile (upper quartile, lower quartile), and the difference was statistically significant (P0.05). Results: the expression of TLR4 in ischemic necrotic myocardium in operation group was significantly higher than that in sham operation group (P < 0.05). The expression of TLR4 in myocardial tissue in treatment group was lower than that in operation group (P < 0.05), but higher than that in sham operation group (P < 0.05). Conclusion 1. The expression of TLR4 was upregulated rapidly after acute myocardial infarction, suggesting that TLR4 may play an important role in the pathogenesis of acute myocardial infarction and may act as an important inflammatory receptor to mediate myocardial ischemic inflammatory injury. Autologous bone marrow stromal stem cells can survive after transplantation in myocardial tissue with acute myocardial infarction. Autologous bone marrow stromal stem cells can be transplanted into auricular vein to treat acute myocardial infarction. One of the mechanisms may be related to the inhibition of TLR4-mediated inflammatory response. It can inhibit the synthesis and release of inflammatory factors involved in TLR 4-mediated inflammatory response to some extent.
【学位授予单位】:大连医科大学
【学位级别】:硕士
【学位授予年份】:2013
【分类号】:R542.22

【参考文献】

相关期刊论文 前9条

1 王同成,唐元升;急性冠脉综合征的研究进展[J];山东医药;2004年31期

2 任美玉;吴欣怡;;Toll样受体的研究进展[J];现代免疫学;2006年04期

3 单守杰,陈绍良,刘煜昊,方五旺,叶飞,段宝祥,张俊杰,林松;自体骨髓间质干细胞移植对梗死心肌的修复作用[J];中国临床康复;2005年07期

4 杨晶;姜德建;张一帅;李元建;胡长平;;Toll样受体与心脏疾病[J];中国药理学通报;2008年09期

5 郭爱桃,韦立新,石怀银,李向红,游联璧;基质金属蛋白酶1与冠状动脉粥样硬化斑块破裂的关系[J];中华病理学杂志;2000年04期

6 马克娟,马克威,赵利华;Toll样受体4和肿瘤坏死因子αmRNA在动脉粥样硬化中表达的相关性研究[J];中华心血管病杂志;2004年10期

7 杨敏,阎纯英,吴贤仁,黄林喜,陈畅,张钰,陈广玲,李玉光;骨髓干细胞动员后归巢梗死心肌机制的研究[J];中国急救医学;2005年03期

8 闫少西;王勇;;Toll样受体与心血管疾病[J];中日友好医院学报;2009年03期

9 连锋,朱洪生,黄日太,郑家豪,吴学军,张谷兰,王小妹;骨髓间质干细胞移植梗死心肌后细胞因子分泌及对血管新生的影响[J];中国胸心血管外科临床杂志;2004年01期



本文编号:2098792

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/jjyx/2098792.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户6cc67***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com