首页|微小RNA-30a调控丝裂原活化蛋白激酶通路对主动脉夹层大鼠的影响

微小RNA-30a调控丝裂原活化蛋白激酶通路对主动脉夹层大鼠的影响

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目的 探讨微小RNA(miR)-30a调控MAPK通路对主动脉夹层大鼠模型夹层形成、炎性因子及血管收缩的影响。方法 选取SD大鼠 50 只,建立主动脉夹层大鼠模型,将其随机分为对照组、模型组、miR-NC组、miR-30a组、miR-30a抑制剂组,各组 10 只。组织病理学染色观察大鼠主动脉组织变化、主动脉中膜弹力纤维与胶原纤维变化;采用PCR、尾动脉压力计、ELISA法对各组miR-30a表达、干预前后收缩压情况、血清炎性因子表达进行检测;采用Western blotting检测各组大鼠基质金属蛋白酶(MMP)-6、MMP-2 蛋白表达以及MAPK通路相关蛋白表达。结果 MiR-30a抑制剂组血管壁撕裂程度和内动脉壁排列紊乱有所改善;miR-30a抑制剂组改善血管重构;与对照组相比,模型组miR-30a表达较高,与miR-NC组相比,miR-30a组、miR-30a抑制剂组表达较低,P<0。05;干预前,各组收缩压比较差异无统计学意义,P>0。05;与对照组相比,模型组收缩压较高,与miR-NC组相比,miR-30a组表达较高,miR-30a抑制剂组表达较低,P<0。05;与对照组相比,模型组肿瘤坏死因子(TNF)、白细胞介素(IL)-6、IL-1β表达较高,与miR-NC组相比,miR-30a组表达较高,miR-30a抑制剂组表达较低,P<0。05;与对照组相比,模型组、MMP-6、MMP-2、Ras、Raf、P38 MAPK及ERK1/2 蛋白表达较高,与miR-NC组相比,miR-30a组表达较高,miR-30a抑制剂组表达较低,P<0。05。结论 MiR-30a参与主动脉夹层的形成、炎症反应、调控主动脉夹层血管重构,可能是通过调控MAPK信号通路实现的。
Effect of microRNA-30a regulation of mitogen-activated protein kinase pathway on aortic coarctation in rats
Objective To investigate the effects of microRNA(miR)-30a-regulated MAPK pathway on the formation of intercalation,inflammatory factors and vasoconstriction in a rat model of aortic coarctation.Methods Fifty SD rats were selected to establish the rat model of aortic coarctation,and were randomly divided into control group,model group,miR-NC group,miR-30a group and miR-30a inhibitor group,10 rats in each group.Histopathological changes in the aortic tissue and changes in the elastic fibers and collagen fibers of the aortic mesothelium were observed;The expression of miR-30a,systolic blood pressure before and after the intervention and the expression of serum inflammatory factors in each group were measured by PCR,tail artery manometry and ELISA;Matrix metalloproteinase(MMP)-6,MMP-2 protein expression and MAPK pathway were measured by Western blotting in each group.The expression of MMP-6,MMP-2 and MAPK pathway related proteins were measured by Western blotting.Results The miR-30a inhibitor group improved the degree of vessel wall tearing and disorganized internal arterial wall arrangement;The miR-30a group improved vascular remodeling;miR-30a expression was higher in the model group compared with the control group,and lower in the miR-30a group and miR-30a inhibitor group compared with the miR-NC group,P<0.05;Before the intervention,the difference in systolic blood pressure between the groups compared was not statistically significant,P>0.05;Compared with the control group,systolic blood pressure was higher in the model group,higher expression in the miR-30a group and lower expression in the miR-30a inhibitor group compared with the miR-NC group,P<0.05;compared with the control group,tumor necrosis factor(TNF)-α,interleukin(IL)-6,IL-1β expression was higher in the model group,higher expression in the miR-30a group compared with the miR-NC group,lower expression in the miR-30a inhibitor group,P<0.05;higher expression of TNF-α,MMP-6,MMP-2,Ras,Raf,P38 MAPK,ERK1/2 proteins in the model group compared with the control group,higher expression in the miR-30a group compared with the miR-NC group,lower expression in the miR-30a inhibitor group,P<0.05.Conclusion MiR-30a is involved in the process of aortic coarctation formation,inflammatory response,and regulation of aortic coarctation vascular remodeling,possibly through regulation of the MAPK signaling pathway.

MicroRNA-30aMitogen-activated protein kinase pathwayAortic coarctationWestern blottingRat

吴跃武、胡斌、过小冬、付琴、邹志佳

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江西省抚州市第一人民医院心胸外科,江西 抚州 344000

江西省抚州市第一人民医院检验科,江西 抚州 344000

微小RNA-30a 丝裂原活化蛋白激酶通路 主动脉夹层 免疫印迹法 大鼠

江西省卫生健康委科技项目

202212875

2024

解剖学报
中国解剖学会

解剖学报

CSTPCD
影响因子:0.462
ISSN:0529-1356
年,卷(期):2024.55(2)
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