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铜离子电化学疗法通过诱导产生Caspase-3介导的细胞凋亡促进混合痔的痔区血管萎缩与闭塞的机制
汪敏,谢振年,安晓静,蔡梦涵,赵卫兵,贾泽媛,甘沛艳
中国中医科学院西苑医院 肛肠科北京 100091;中国中医科学院西苑医院 病理科北京 100091
摘要:
目的:探讨铜离子电化学疗法(ECTCI)在中医枯痔钉理论基础上对混合痔患者痔区血管结构及细胞凋亡通路的影响,揭示其治疗机制。方法:选取2022年7月—2023年2月中国中医科学院西苑医院肛肠科收治的混合痔患者40例,采用随机数字表法分为对照组、观察1组、观察2组、观察3组,每组各10例。观察1组治疗280 s,观察2组治疗560 s,观察3组治疗840 s,对照组不予ECTCI治疗。采用HE染色观察痔组织中血管形态变化,免疫组化检测血小板内皮细胞黏附分子-1(PECAM-1),即CD31及血管内皮生长因子(VEGF)表达,采用RT-PCR和免疫印迹(Western blot)法检测凋亡相关蛋白半胱天冬氨酸蛋白酶-3(Caspase-3)抗体、B细胞淋巴瘤-2(Bcl-2)的mRNA和蛋白表达水平。结果:ECTCI治疗组呈现剂量依赖性地破坏血管结构,表现为微血管密度降低、血管壁断裂及纤维素样坏死。各组间VEGF表达无显著差异。凋亡蛋白检测结果显示,Caspase-3表达随治疗时间延长而上调,而Bcl-2表达随治疗时间延长而下调,提示线粒体凋亡通路被激活。结论:ECTCI治疗混合痔的机制是其通过直接破坏痔区血管内皮结构并激活Caspase-3介导的细胞凋亡通路,促进病理血管萎缩与闭塞。
关键词:    铜离子电化学疗法  细胞凋亡  血管重塑  半胱天冬氨酸蛋白酶-3
DOI:10.3969/j.issn.1007-6948.2026.04.003
投稿时间:2026-01-07
基金项目:国家自然科学基金(81072813);中国中医科学院科技创新工程(C12021A02116);北京市海淀区卫生健康发展科研培育计划(2025XLA065-2)
Electro-chemical therapy by cupric ion promotes vascular atrophy and occlusion in mixed hemorrhoids through caspase-3-mediated apoptosis
WANG Min,XIE Zhen-nian,AN Xiao-jing
Abstract:
Objective To investigate the effects of electro-chemical therapy by cupric ion (ECTCI), based on the theory of necrotizing hemorrhoid ligation in Traditional Chinese Medicine, on the vascular structure and apoptotic pathways in the hemorrhoidal tissues of patients with mixed hemorrhoids, and to elucidate its therapeutic mechanism. Methods Forty patients with mixed hemorrhoids were selected and randomly assigned to a control group and three ECTCI treatment groups with different treatment durations (280 s, 560 s, 840 s). Hematoxylin and eosin (HE) staining was used to observe morphological changes in blood vessels. Immunohistochemistry was performed to detect the expression of CD31 and VEGF. RT-PCR and Western blot were employed to analyze the mRNA and protein expression levels of the apoptosis-related proteins Caspase-3 and Bcl-2. Results The ECTCI treatment groups exhibited dose-dependent destruction of vascular structures, manifested as reduced microvessel density, ruptured vessel walls, and fibrinoid necrosis. No significant difference in VEGF expression was observed among the groups. Apoptosis-related analyses revealed that Caspase-3 expression was up-regulated with increasing treatment duration, while Bcl-2 expression was down-regulated, suggesting activation of the mitochondrial apoptotic pathway. Conclusion ECTCI promotes the atrophy and occlusion of pathological vessels by directly damaging the vascular endothelial structure in hemorrhoidal tissues and activating the Caspase-3-mediated apoptotic pathway, which represents a key mechanism in its treatment of mixed hemorrhoids.
Key words:  Hemorrhoids  electro-chemical therapy by cupric ion  apoptosis  vascular remodeling  Caspase-3

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