| 赵霞,李丹阳,苏莉,等.不同气压强度对创伤性深静脉血栓形成及 NLRP3/caspase1通路的影响[J].安徽医药,2025,29(9):1828-1832. |
| 不同气压强度对创伤性深静脉血栓形成及 NLRP3/caspase1通路的影响 |
| Effects of different air pressure intensities on traumatic deep vein thrombosis and NLRP3/caspase1 pathway |
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| DOI：10.3969/j.issn.1009-6469.2025.09.027 |
| 中文关键词: 深静脉血栓形成 气压 压强 间歇充气加压 强度 内皮细胞功能 炎症 焦亡 |
| 英文关键词: Deep vein thrombosis Air pressure Pressure function Inflammation Focal death |
| 基金项目:河北省医学科学研究课题计划项目( 20232201) |
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| 中文摘要: |
| 目的探讨不同强度的间歇充气加压( IPC)治疗对创伤性深静脉血栓形成( DVT)模型大鼠 DVT形成的影响，并初步探讨可能的潜在机制。方法研究时间为 2023年 3―10月。采用血管钳夹股静脉 +双后肢固定制动的方式构建创伤性 DVT大鼠模型。 24只成功造模的模型大鼠采用随机数字表法分为三组:模型组(仅佩带 IPC袖带，不施加压力)低强度组(IPC袖带施加 120 mmHg压力)、高强度组( IPC袖带施加 200 mmHg压力)，每组 8只。假手术组( n=8)只分离出股静脉，、不作夹血管操作。酶联免疫吸附分析检测血管内皮细胞损伤标志物可溶性血栓调节蛋白( sTM)、内皮素 -1(ET-1)、一氧化氮(NO)、血管内皮生长因子( VEGF)、内皮一氧化氮合酶( eNOS)的水平，以及炎症介质 C反应蛋白(CRP)、白细胞介素 -18(IL-18)肿瘤坏死因子 α(TNF-α)白细胞介素 -1β(IL-1β)的水平。蛋白质印迹法分析 NOD样受体热蛋白结构域相关蛋白 3(NLRP3)/胱天、蛋白酶 -1(caspase-1)相、关蛋白表达。结果与模型组相比，低强度组和高强度组大鼠血栓湿重［(11.54±0.94)mg、(7.12±1.08)mg比( 15.75±1.33) mg］、血浆 sTM、NO和 ET水平、血清 CRP、IL-18、IL-1β和 TNF-α水平，以及股静脉血管内皮组织中 NLRP3、ASC、cleaved caspase-1蛋白表达均显著降低，而 eNOS和 VEGF水平显著升高( P<0.05)；与低强度组相比，高强度组大鼠血栓湿重、血浆 sTM、NO和 ET水平、血清 CRP、IL-18、IL-1β和 TNF-α水平，以及股静脉血管内皮组织中 NLRP3、ASC、cleaved caspase-1蛋白表达均显著降低，而 eNOS和 VEGF水平显著升高(P<0.05)。结论不同强度 IPC治疗能够通过抑制炎症反应和保护血管内皮细胞功能来抑制大鼠 DVT形成，这可能是通过抑制 NLRP3/caspase-1介导的细胞焦亡来实现。 |
| 英文摘要: |
| Objective To investigate the effects of different intensities of intermittent pneumatic compression (IPC) treatment on theformation of deep vein thrombosis (DVT) in a rat model of traumatic DVT, and to explore the possible underlying mechanisms.Meth. ods The study was conducted from March to October 2023. A rat model of traumatic DVT was constructed by clamping the femoralvein with vascular forceps plus bilateral hind limb immobilization. Twenty-four successfully modeled rats were randomly assigned intothree groups: model group (only wearing IPC cuff, no pressure applied), low-intensity group (120 mmHg pressure applied by IPC cuff), and high-intensity group (200 mmHg pressure applied by IPC cuff), with 8 rats in each group. In the sham operation group (n=8), only the femoral vein was isolated without clamping operation. Enzyme-linked immunosorbent assay was used to detect the levels of markersof vascular endothelial cell injury, soluble thrombomodulin (sTM), endothelin-1 (ET-1), nitric oxide (NO), vascular endothelial growthfactor (VEGF), and endothelial nitric oxide synthase (eNOS), as well as the levels of inflammatory mediators C-reactive protein (CRP), interleukin-18 (IL-18), tumor necrosis factor-α ( TNF-α), and interleukin-1β (IL-1β). Protein immunoblotting was performed to analyze the expression of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3)/cysteine aspartate protease-1 (caspase-1)-re-lated proteins.Results Compared with the model group, the thrombus wet weight [(11.54±0.94) mg, (7.12±1.08) mg vs. (15.75±1.33) mg], plasma sTM, NO, and ET levels, serum CRP, IL-18, IL-1β, and TNF-α levels, and NLRP3, ASC, and cleaved caspase-1 protein expression levels in the endothelial tissues of femoral vein vessels of rats in the low-intensity and high-intensity groups were significant-ly reduced, while eNOS and VEGF levels were significantly increased (P<0.05). Compared with the low-intensity group, rats in the high-intensity group had significantly lower thrombus wet weight, plasma sTM, NO, and ET levels, serum CRP, IL-18, IL-1β, and TNF-α levels, as well as NLRP3, ASC, and cleaved caspase-1 protein expression levels in femoral vein vascular endothelial tissues, whereasthe levels of eNOS and VEGF were significantly higher (P<0.05).Conclusion Different intensities of IPC treatment were able to inhib-it DVT formation in rats by suppressing the inflammatory response and protecting the function of vascular endothelial cells, which maybe achieved by inhibiting NLRP3/caspase-1-mediated cellular pyroptosis. |
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