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作 者:赵凯[1] 陈文强[1] 徐兴晟 孟晓[1] 张运[1] 李继福[1]
机构地区:[1]山东大学齐鲁医院心内科,山东省济南市250012
出 处:《中国动脉硬化杂志》2014年第1期37-42,共6页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金资助(30971216)
摘 要:目的研究人外周血单核细胞的自体吞噬与冠状动脉粥样硬化斑块易损性的关系。方法对40例稳定型心绞痛(SAP)患者及40例急性冠状动脉综合征(ACS)患者行冠状动脉造影和血管内超声检查。应用Western blot技术检测两组患者外周血单核细胞的Beclin-1蛋白、微管相关蛋白1轻链3(MAP1-LC3)及自噬相关蛋白Atg5-Atg12复合物的表达量,应用激光共聚焦显微镜检测自噬特异性蛋白MAP1-LC3在单核细胞内的表达量。结果血管内超声检测SAP组斑块共计62个,其中纤维性斑块占48%(30/62),而ACS组斑块共计71个,其中脂质性斑块占56%(40/71)。ACS患者外周血单核细胞的Beclin-1、MAP1-LC3Ⅱ及Atg5-Atg12的表达量显著低于SAP组(P<0.01)。结论稳定型心绞痛患者的冠状动脉斑块以较稳定的纤维性斑块为主,而急性冠状动脉综合征患者的冠状动脉斑块以易损质软的脂质性斑块为主,且冠心病患者外周血单核细胞的自体吞噬随着冠状动脉粥样硬化斑块的不稳定性的增加而降低,增强外周血单核细胞的自体吞噬可能成为稳定冠状动脉粥样硬化斑块,减少急性冠状动脉事件,降低死亡风险的一个潜在的治疗靶点。Aim To elucidate the relationship between autophagy of peripheral blood monocyte (PBM) and the vulnerability of atheroselerotic plaques. Methods Forty patients with stable angina pectoris (SAP), 40 patients with acute coronary syndrome (ACS) compromised the study groups. All patients underwent coronary angiography (CAG) and intravascular ultrasound (IViSS) examinations. The expression levels of autophagy related protein Beclin-1, mierotubule- associated protein 1 light chain 3 ( MAP1 -LC3 ) and Atg5-Atgl2 complex in PBM were detected by Western blot. MAP1- LC3 ( autophagy-specific protein) in the PMB was also examined by laser scanning confocal microscope. Results Six-ty two plaques were detected by IVUS in the SAP patients, which included 30 fibrous ones, while 71 plaques were evi denced in the ACS group, which encompassed 40 lipid ones. The expression levels of Beclin-1, MAP1-LC3 and Atg5- Atg12 complex in PBM in ACS patients were significantly lower than those in SAP patients (P 〈 0. 01 ). Conclusion The patients in SAP group had more stable fibrous plaques than those in the ACS group (P 〈 0. 01 ) , while the ACS pa tients had more vulnerable soft lipid ones than those in the SAP group ( P 〈 0.01 ). The autophagy of PBM in patients with coronary heart disease (CHD) decreases with the increasing vulnerability of atherosclerotic plaques. Enhancing the autophagy of PBM may be a potential therapeutic target of stabilizing atherosclerotic plaques, which will reduce the acute coronary events and lower the mortality of patients with CHD.
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