Wei T, Ding Y, Zhang J, Li J, Zhang H, Kang P, Zhang N
Department of Cardiovascular Medicine of First Affiliated Hospital, Bengbu Medical University, Bengbu 233000, China.
Key Laboratory of Preclinical and Clinical Cardiovascular Medicine, Bengbu Medical University, Bengbu 233000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Feb 20;44(2):308-316. doi: 10.12122/j.issn.1673-4254.2024.02.13.
To analyze the correlation of copper death inducer ferredoxin 1 (FDX1) and lipoic acid (LA) with the occurrence and severity of coronary atherosclerosis and explore their roles in coronary heart disease (CHD).
We analyzed the data of 226 patients undergoing coronary artery angiography (CAG) in our hospital between October, 2021 and October, 2022, including 47 patients with normal CAG findings (control group) and 179 patients with mild, moderate or severe coronary artery stenosis (CHD group). Serum FDX1 and LA levels were determined with ELISA for all the patients. We also examined pathological changes in the aorta of normal and ApoE mice using HE staining and observed collagen fiber deposition with Sirius red staining. Immunohistochemistry was used to detect the expression and distribution of FDX1 and LA in the aorta, and RT-PCR was performed to detect the expressions of FDX1, LIAS and ACO2 mRNAs in the myocardial tissues.
Compared with the control patients, CHD patients had significantly lower serum FDX1 and LA levels, which decreased progressively as coronary artery stenosis worsened ( < 0.01) and as the number of involved coronary artery branches increased ( < 0.05). Serum FDX1 and LA levels were positively correlated (=0.451, < 0.01) and they both negatively correlated with the Gensini score (=-0.241 and -0.273, respectively; < 0.01). Compared with normal mice, ApoE mice showed significantly increased lipid levels ( < 0.01) and atherosclerosis index, obvious thickening, lipid aggregation, and collagen fiber hyperplasia in the aorta, and significantly reduced expressions of FDX1, LA, LIAS, and ACO2 ( < 0.05).
Serum FDX1 and LA levels decrease with worsening of coronary artery lesions, and theirs expressions are correlated with coronary artery lesions induced by hyperlipidemia.
分析铜死亡诱导因子铁氧化还原蛋白1（FDX1）和硫辛酸（LA）与冠状动脉粥样硬化发生及严重程度的相关性，并探讨它们在冠心病（CHD）中的作用。
分析我院2021年10月至2022年10月期间226例行冠状动脉造影（CAG）患者的数据，包括47例CAG结果正常的患者（对照组）和179例轻、中、重度冠状动脉狭窄患者（冠心病组）。采用酶联免疫吸附测定法（ELISA）测定所有患者血清FDX1和LA水平。我们还使用苏木精-伊红（HE）染色检查正常小鼠和载脂蛋白E（ApoE）小鼠主动脉的病理变化，并用天狼星红染色观察胶原纤维沉积情况。采用免疫组织化学法检测主动脉中FDX1和LA的表达及分布，并进行逆转录-聚合酶链反应（RT-PCR）检测心肌组织中FDX1、硫辛酸合成酶（LIAS）和乌头酸酶2（ACO2）mRNA的表达。
与对照组患者相比，冠心病患者血清FDX1和LA水平显著降低，随着冠状动脉狭窄程度加重（<0.01）以及受累冠状动脉分支数量增加（<0.05），其水平逐渐下降。血清FDX1和LA水平呈正相关（=0.451，<0.01），且二者均与Gensini评分呈负相关（分别为=-0.241和-0.273；<0.01）。与正常小鼠相比，ApoE小鼠血脂水平显著升高（<0.01），动脉粥样硬化指数升高，主动脉明显增厚、脂质聚集和胶原纤维增生，且FDX1、LA、LIAS和ACO2表达显著降低（<0.05）。
血清FDX1和LA水平随冠状动脉病变加重而降低，其表达与高脂血症诱导的冠状动脉病变相关。
