坏死在高氧诱导的青春期前大鼠急性肺损伤中的作用

Q4 Medicine
Haibing Lu, Yingping Jia, W. Yuan, Y. Qiu, R. Zhou
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引用次数: 0

摘要

目的探讨坏死在高氧诱导的青春期前大鼠急性肺损伤(ALI)中的作用。方法将72只清洁级健康雄性Sprague-Dawley大鼠,年龄14天,体重40~50g,采用随机数表法分为3组(每组24只):对照组(C组)、高氧诱导的ALI组(ALI组)和高氧诱导ALI和坏死抑制素-1组(ALI+n组)。ALI+N组大鼠腹腔注射坏死抑素1.0mg/kg,每日1次,连续3天。C组和ALI组大鼠腹腔注射二甲基亚砜0.2ml/kg,每天一次,连续3天。吸入氧气后72小时处死动物,收集支气管肺泡灌洗液(BALF)测定白细胞介素-6(IL-6)和IL-8浓度(酶联免疫吸附法)、超氧化物歧化酶(SOD)活性(黄嘌呤氧化酶法)和丙二醛(MDA)浓度(硫代巴比妥酸法)。取肺组织测量湿/干重比(W/D比),并检查肺组织的病理变化(用光学显微镜)和超微结构(用电子显微镜)。计算肺泡损伤率(IAR)。Western blot检测受体相互作用蛋白激酶1(RIPK1)、RIPK3和混合谱系激酶结构域样蛋白(MLKL)在肺组织中的表达。结果与C组相比,ALI组BALF中IL-6、IL-8和MDA浓度显著升高,SOD活性下降,肺组织W/D比和IAR升高,RIPK1、RIPK3和MLKL表达上调(P<0.05),病理损伤加重。与ALI组相比,BALF中IL-6、IL-8和MDA浓度显著降低,SOD活性升高,肺组织W/D比和IAR降低,RIPK1、RIPK3和MLKL表达下调(P<0.05),结论坏死参与了高氧诱导的大鼠ALI的病理生理过程。关键词:坏死;婴儿;高氧血症;急性肺损伤
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of necroptosis in hyperoxia-induced acute lung injury in preadolescent rats
Objective To evaluate the role of necroptosis in hyperoxia-induced acute lung injury (ALI) in preadolescent rats. Methods A total of 72 clean-grade healthy male Sprague-Dawley rats, aged 14 days, weighing 40-50 g, were divided into 3 groups (n=24 each) by using a random number table method: control group (group C), hyperoxia-induced ALI group (group ALI) and hyperoxia-induced ALI and necrostatin-1 group (group ALI+ N). The rats of group ALI+ N was intraperitoneally injected with necrostatin-1 1.0 mg/kg once a day for 3 consecutive days.The rats were intraperitoneally injected with dimethyl sulfoxide 0.2 ml/kg once a day for 3 consecutive days in C and ALI groups.The animals were sacrificed at 72 h after inhaling oxygen, and bronchoalveolar lavage fluid (BALF) was collected for determination of interleukin-6 (IL-6) and IL-8 concentrations (by enzyme-linked immunosorbent assay), superoxide dismutase (SOD) activity (by xanthine oxidase method), and malondialdehyde (MDA) concentration (by thiobarbituric acid method). Lung tissues were taken for measurement of wet/dry weight ratio (W/D ratio) and for examination of the pathological changes (with a light microscope) and ultrastructure of lung tissues (with an electron microscope). The injured alveolus rate (IAR) was calculated.The expression of receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed-lineage kinase domain-like protein (MLKL) in lung tissues was detected by Western blot. Results Compared with group C, the concentrations of IL-6, IL-8 and MDA in BALF were significantly increased, the activity of SOD in BALF was decreased, the W/D ratio and IAR of lung tissues were increased, the expression of RIPK1, RIPK3 and MLKL in lung tissues was up-regulated (P<0.05), and the pathological damage was accentuated in group ALI.Compared with group ALI, the concentrations of IL-6, IL-8 and MDA in BALF were significantly deceased, the activity of SOD in BALF was increased, the W/D ratio and IAR of lung tissues were decreased, the expression of RIPK1, RIPK3 and MLKL in lung tissues was down-regulated (P<0.05), and the pathological damage was significantly attenuated in group ALI+ N. Conclusion Necroptosis is involved in the pathophysiological process of hyperoxia-induced ALI in preadolescent rats. Key words: Necrosis; Infant; Hyperoxia; Acute lung injury
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中华麻醉学杂志
中华麻醉学杂志 Medicine-Anesthesiology and Pain Medicine
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