慢性间歇低氧对大鼠肺组织损伤及依达拉奉的干预作用

发布时间：2018-07-09 09:06

  本文选题：睡眠呼吸暂停低通气综合征 + 阻塞性　； 参考：《临床耳鼻咽喉头颈外科杂志》2015年19期

【摘要】：目的:探讨慢性间歇低氧(CIH)对大鼠肺损伤的机制和依达拉奉的干预作用及可能机制。方法:采用随机数字表法将96只雄性Wistar大鼠随机分为正常对照组(UC组)、间歇低氧组(CIH组)、依达拉奉治疗组(NE组)、低氧生理盐水组(NS组),各亚组持续时间分别为1、2、3、4周,每个亚组6只大鼠。实验结束后分别观察各亚组大鼠肺组织苏木精-伊红病理变化、血气检测血氧分压(PO2),采用化学法检测肺组织MDA含量和SOD活性,实时荧光定量PCR检测AngⅡmRNA。结果:UC组未见明显病理损害,而CIH组肺泡壁水肿增厚,肺泡融合,肺间质及支气管上皮内也可见中性粒细胞浸润,且随时间延长,病理损伤逐渐加重;与NS组相比,NE组出现病理损伤的时间较晚且程度较轻;各组亚组内PO2未见差异;与UC组同一时间点比较,CIH组PO2明显降低,而NE组较NS组有所恢复;与UC及NE组比较,CIH组及NS组MDA含量于各个时间点均逐渐增加(P0.05),SOD活性于各个时间点均逐渐减少(P0.05);AngⅡmRNA的表达于各个时间点增加,于4周达高峰;与CIH组比较,NE组各指标的变化过程受到抑制(P0.05)。CIH组AngⅡmRNA与SOD呈负相关(r=-0.904,P0.01);AngⅡmRNA与MDA呈正相关(r=0.782,P0.01)。结论:慢性间歇低氧可通过氧化应激和激活AngⅡ导致肺组织损伤,依达拉奉可能通过清除氧自由基,从而抵抗间歇低氧所致肺损伤。
[Abstract]:Aim: to investigate the mechanism of chronic intermittent hypoxia (CIH) on lung injury in rats and the possible mechanism of Edaravone. Methods: 96 male Wistar rats were randomly divided into normal control group (UC group), intermittent hypoxia group (CIH group), Edaravone treatment group (NE group) and hypoxic saline group (NS group). There were 6 rats in each subgroup. After the experiment, the pathological changes of hematoxylin and eosin in lung tissue of rats in each subgroup were observed. Blood gas was used to detect the partial pressure of oxygen (PO2), the content of MDA and the activity of SOD in lung tissue were detected by chemical method, and the Ang 鈪，

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