Department of Vascular Surgery, Shaanxi Provincial People's Hospital, 256 Youyixi Road, Xi'an, 710068, Shaanxi, China.
Department of Cardiovascular Surgery, Shaanxi Provincial People's Hospital, 256 Youyixi Road, Xi'an, 710068, Shaanxi, China.
Sci Rep. 2023 Dec 7;13(1):21574. doi: 10.1038/s41598-023-48858-z.
Lower limb ischemia-reperfusion is a common pathological process during clinical surgery. Because lower limb ischemia-reperfusion usually aggravates ischemia-induced skeletal muscle tissue injury after lower limb ischemia-reperfusion, it also causes remote organ heart, intestine, liver, lung and other injuries, and there is no effective clinical treatment for lower limb ischemia-reperfusion injury, so it is urgent to study its injury mechanism. In this study, the rat model of lower limb ischemia-reperfusion was established by clamping the femoral artery with microarterial clips, and the wall destruction such as intimal injury, cell edema, collagen degeneration, neutrophil infiltration, and elastic fiberboard injury of the femoral artery wall was detected. The expression of inflammatory factors was detected by immunohistochemistry. miR-206 preconditioning was used to observe the expression of inflammatory factors, redox status and apoptosis in the vascular wall of rats after acute limb ischemia-reperfusion. Our findings suggest that vascular endothelial cell edema increases, wall thickening, neutrophil infiltration, and elastic fiber layer damage during IRI. Inflammatory factor expression was increased in femoral artery tissue, and miR-206 expression levels were significantly down-regulated. Further studies have found that miR-206 attenuates lower limb IRI by regulating the effects of phase inflammatory factors. In this study, we investigated the effect of miR-206 on inflammatory factors and its possible role in the development of lower limb IRI, providing new research ideas for the regulatory mechanism of lower limb IRI, and providing a certain theoretical basis for the treatment of lower limb ischemia-reperfusion injury after surgery or endovascular intervention.
肢体缺血再灌注是临床手术中常见的病理过程。由于肢体缺血再灌注后通常会加重肢体缺血引起的骨骼肌组织损伤，还会引起心脏、肠、肝、肺等远隔器官的损伤，且目前对于肢体缺血再灌注损伤尚无有效的临床治疗方法，因此研究其损伤机制迫在眉睫。本研究通过微动脉夹夹闭股动脉建立大鼠肢体缺血再灌注模型，检测股动脉壁的内膜损伤、细胞水肿、胶原变性、中性粒细胞浸润、弹性纤维板损伤等壁破坏情况，并通过免疫组化检测炎症因子的表达。采用 miR-206 预处理，观察急性肢体缺血再灌注后大鼠血管壁中炎症因子、氧化还原状态和细胞凋亡的表达。结果发现，在 IRI 过程中，血管内皮细胞水肿增加，壁增厚，中性粒细胞浸润，弹性纤维层受损。股动脉组织中炎症因子表达增加，miR-206 表达水平明显下调。进一步研究发现，miR-206 通过调控相炎症因子的作用来减轻肢体 IRI。本研究探讨了 miR-206 对炎症因子的作用及其在肢体 IRI 发生发展中的可能作用，为肢体 IRI 的调控机制提供了新的研究思路，为手术或血管内介入治疗后肢体缺血再灌注损伤的治疗提供了一定的理论依据。
