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[目的]探讨镉中毒对血管内皮细胞凋亡的病理机制,为进一步揭示环境毒邪所致血管衰老以及冠心康颗粒剂的防护作用,从而为血管衰老的预防和控制提供理论依据。[方法]通过人脐静脉内皮细胞培养,分成六组,建立不同浓度氯化镉的模型组和西药(硫酸锌)、中药复方(冠心康颗粒剂低、中、高浓度)的处理组后,继续培养24h、48h,观察Bcl-2含量、BAX蛋白含量和Caspase-3酶活性变化。[结果]不同浓度氯化镉作用24h、48h后,与对照组比较,各组的Bcl-2含量降低、BAX蛋白含量升高、Caspase-3酶活性增强(P<0.05)。西、中药复方处理组与模型组比较,Bcl-2含量升高、BAX蛋白含量下降、Caspase-3酶活性降低(P<0.05)。随着氯化镉浓度不同,西、中药复方处理组的表现有差异。[结论]镉中毒可造成血管内皮细胞病理损伤,也可引起衰老。硫酸锌和中药复方冠心康颗粒剂对血管内皮细胞镉毒作用具有一定的保护作用,从而可能延缓衰老。
[Objective] To explore the pathological mechanism of cadmium poisoning on vascular endothelial cell apoptosis and to provide a theoretical basis for the prevention and control of vascular aging in order to further reveal the vascular aging induced by environmental poison and the protective effect of Guanxinkang granules. [Method] The human umbilical vein endothelial cells were cultured and divided into six groups. After the establishment of different concentrations of cadmium chloride model group and Western medicine (zinc sulfate), Chinese medicine compound (Guanxinkang granules low, medium and high concentration) , Continue to train 24h, 48h, observe the Bcl-2 content, BAX protein content and Caspase-3 activity changes. [Result] Compared with the control group, the contents of Bcl-2 and BAX protein increased and the activity of Caspase-3 increased (P <0.05) at different concentrations of cadmium chloride for 24h and 48h. Compared with the model group, the content of Bcl-2, the content of BAX protein decreased and the activity of Caspase-3 decreased (P <0.05). With the different concentrations of cadmium chloride, western and traditional Chinese medicine compound treatment group performance differences. [Conclusion] Cadmium poisoning can cause pathological damage of vascular endothelial cells and may also cause aging. Zinc sulfate and traditional Chinese medicine compound Guanxinkang granules have a certain protective effect on the cadmium toxicity of vascular endothelial cells, which may delay aging.