CAJ | 학술논문

目的：通过对慢性间断低氧(CIH)大鼠动脉内膜病理改变及厚度的观察和血管炎症因子变化的检测，探讨CIH对动脉内膜的损伤及其可能的途径。方法：24只成年Sprague-Dawley雄性大鼠随机分为4组：慢性间断低氧组(CIH组)，慢性间断低氧+N-乙酰半胱氨酸干预组(CIH+NAC组)、慢性间断低氧+生理盐水组(CIH+NS组)和常氧对照组(control组)，每组6只。经相应处理42 d后处死大鼠取心脏血和胸主动脉。ELISA法检测低氧诱导因子-1α(HIF-1α)，氧化低密度脂蛋白(ox-LDL)，正五聚蛋白3(PTX3)血清浓度，观察胸主动脉病理变化，通过计算机图像分析系统测定动脉内膜厚度。结果：CIH组及CIH+NS组大鼠胸主动脉内皮细胞部分受损脱落，少量单核细胞、巨噬细胞浸润，动脉内膜厚度与对照组比较均明显增厚(P<0.001)；CIH+NAC组大鼠胸主动脉内膜厚度与CIH组及CIH+NS组比较显著减小(P<0.001)。CIH组及CIH+NS组大鼠血清HIF-1α，ox-LDL，PTX3浓度与对照组比较明显增高(P<0.001)。CIH+NAC组大鼠血清HIF-1α，ox-LDL，PTX3水平较CIH组及CIH+NS组明显降低(P<0.001)。大鼠血清HIF-1α，ox-LDL，PTX3浓度间呈正相关，ox-LDL，PTX3浓度与胸主动脉内膜厚度呈正相关(P<0.001)。结论：CIH可损伤血管内皮细胞，使动脉内膜增厚。CIH通过激活氧化应激状态，增加HIF-1α，ox-LDL，PTX3等因子的产生是导致血管内皮损伤的一个重要途径。
목적：통과대만성간단저양(CIH)대서동맥내막병리개변급후도적관찰화혈관염증인자변화적검측，탐토CIH대동맥내막적손상급기가능적도경。방법：24지성년Sprague-Dawley웅성대서수궤분위4조：만성간단저양조(CIH조)，만성간단저양+N-을선반광안산간예조(CIH+NAC조)、만성간단저양+생리염수조(CIH+NS조)화상양대조조(control조)，매조6지。경상응처리42 d후처사대서취심장혈화흉주동맥。ELISA법검측저양유도인자-1α(HIF-1α)，양화저밀도지단백(ox-LDL)，정오취단백3(PTX3)혈청농도，관찰흉주동맥병리변화，통과계산궤도상분석계통측정동맥내막후도。결과：CIH조급CIH+NS조대서흉주동맥내피세포부분수손탈락，소량단핵세포、거서세포침윤，동맥내막후도여대조조비교균명현증후(P<0.001)；CIH+NAC조대서흉주동맥내막후도여CIH조급CIH+NS조비교현저감소(P<0.001)。CIH조급CIH+NS조대서혈청HIF-1α，ox-LDL，PTX3농도여대조조비교명현증고(P<0.001)。CIH+NAC조대서혈청HIF-1α，ox-LDL，PTX3수평교CIH조급CIH+NS조명현강저(P<0.001)。대서혈청HIF-1α，ox-LDL，PTX3농도간정정상관，ox-LDL，PTX3농도여흉주동맥내막후도정정상관(P<0.001)。결론：CIH가손상혈관내피세포，사동맥내막증후。CIH통과격활양화응격상태，증가HIF-1α，ox-LDL，PTX3등인자적산생시도치혈관내피손상적일개중요도경。
Objective:To examine the pathological change and intima thickness of thoracic aorta, detect the serum concentration of hypoxia-inducible factor-1α(HIF-1α), oxidized LDL (ox-LDL), and pentraxin 3 (PTX3) in the rat model of chronic intermittent hypoxia (CIH), and to determine the effect of CIH on endarterium injury and its possible pathway.Methods:Twenty-four male Sprague-Dawley (SD) rats were divided into 4 groups:a CIH+N-acetylcysteine (NAC) group, a CIH+normal saline (NS) group, a CIH control group and a control group. CIH rats were subjected to alternating cycles of hypoxia (6%-8%O2 in N2 for 20-25 s) and normoxia (21%O2 in N2 for 2 min) every 180 s for 7 h/d. Rats in the control group were not treated. Rats in the CIH+NAC group were treated with NAC [800 mL/(kg.d)] intraperitoneal injection, and rats in the CIH+NS group were treated with NS [5 mL/(kg.d)] intraperitoneal injection. Atfer 42 day treatment, the rats were sacriifced, blood taken, and thoracic aorta cut off. hTe serum concentration of HIF-1α, ox-LDL, and PTX3 were detected by ELISA. hTe thickness of intima was taken by computer digital image analysis. Results:Vascular endothelial cell injury and detachment were found in the thoracic aorta in the CIH and the CIH+NS group. The intima in the CIH and the CIH+NS group was thicker than that in the control and the CIH+NAC group (P<0.001). The serum concentration of HIF-1α, ox-LDL, and PTX3 in the CIH and the CIH+NS group was higher than that in the control and the CIH+NAC group (P<0.001). The serum concentration of HIF-1α, ox-LDL, and PTX3 was pairwise positive correlation, and the serum concentration of ox-LDL and PTX3 was positively correlated with the thickness of intina (P<0.001). Conclusion:hTe vascular endothelial cell injury and endarterium thickening can be induced by CIH. It is an important pathway that CIH activates oxidative stress and elevates the levels of HIF-1α, ox-LDL, and PTX3.