[1]李萌萌,王 宁.半乳糖凝集素-1对高氧诱导急性肺损伤新生鼠的保护作用及机制研究[J].陕西医学杂志,2021,50(12):1487-1491.[doi:DOI:10.3969/j.issn.1000-7377.2021.12.005]
　LI Mengmeng,WANG Ning.Protective effect and mechanism of galectin-1 on hyperoxia-induced acute lung injury in neonatal rats[J].,2021,50(12):1487-1491.[doi:DOI:10.3969/j.issn.1000-7377.2021.12.005]
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半乳糖凝集素-1对高氧诱导急性肺损伤新生鼠的保护作用及机制研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
50
期数:
2021年12期
页码:
1487-1491
栏目:
基础研究
出版日期:
2021-12-05

文章信息/Info

Title:
Protective effect and mechanism of galectin-1 on hyperoxia-induced acute lung injury in neonatal rats
作者:
李萌萌; 王 宁
(西安大兴医院儿科,陕西 西安 710016)
Author(s):
LI Mengmeng; WANG Ning
(Department of Pediatrics,Xi'an Daxing Hospital,Xi'an 710016,China)
关键词:
急性肺损伤;  半乳糖凝集素-1;  新生鼠;  核因子E2相关因子2;  腺苷酸活化蛋白激酶;  炎症反应;  氧化应激
Keywords:
Acute lung injury;  Galectin-1;  Neonatal rats;  Nuclear factor erythroid-2 related factor 2;  AMP-activated kinase;  Inflammatory reaction;  Oxidative stress
分类号:
R 563
DOI:
DOI:10.3969/j.issn.1000-7377.2021.12.005
文献标志码:
A
摘要:
目的:观察半乳糖凝集素-1(Gal-1)对高氧诱导的急性肺损伤(ALI)新生鼠的保护作用,并探究其可能的作用机制。方法:选取足月新生Wistar大鼠30只,随机分为对照组、高氧组和高氧+Gal-1组,每组10只。对照组大鼠自由呼吸常压空气; 高氧组和高氧+Gal-1组大鼠置于高氧箱中,高氧+Gal-1组大鼠在置于高氧箱前1 h腹腔注射3 μg Gal-1溶液。各组大鼠均在实验开始12 h后处死,取样分析。苏木精-伊红(HE)染色后于光学显微镜下观察肺组织形态。取肺组织,计算干湿比(W/D)。采集支气管肺泡灌洗液(BALF),检测其中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)和白介素-6(IL-6)的表达水平。取部分肺组织,检测其中活性氧(ROS)、超氧化物歧化酶(SOD)和丙二醛(MDA)的表达水平; 采用反转录PCR(RT-PCR)检测其中核因子E2相关因子2(Nrf2)、血红素氧合酶-1(HO-1)、醌氧化还原酶-1(NQO-1)mRNA的表达水平; 采用Western blot检测其中相关蛋白的表达。结果:与高氧组相比,高氧+Gal-1组可见少量纤维渗出或炎性细胞浸润,肺泡损伤程度介于对照组和高氧组之间。高氧组大鼠肺W/D值明显高于对照组,而高氧+Gal-1组大鼠W/D值低于高氧组(均P<0.05)。高氧组大鼠BALF中TNF-α、IL-1β和IL-6的表达水平显著高于对照组,高氧+Gal-1组大鼠的TNF-α、IL-1β和IL-6的表达水平则显著低于高氧组(均P<0.05)。高氧组大鼠肺组织中ROS和MDA的表达水平显著高于对照组,SOD的表达水平显著低于对照组(均P<0.05); 高氧+Gal-1组大鼠ROS和MDA的表达水平显著低于高氧组,SOD的表达水平显著高于高氧组(均P<0.05)。与对照组和高氧组相比,高氧+Gal-1组大鼠肺组织中Nrf2、HO-1和NQO-1 mRNA的表达水平显著升高(均P<0.05)。高氧+Gal-1组的磷酸化腺苷酸活化蛋白激酶(pAMPK)/腺苷酸活化蛋白激酶(AMPK)显著高于对照组和高氧组(均P<0.05)。高氧+Gal-1组Nfr2的表达水平显著高于高氧组(P<0.05); 而在AMPK抑制剂Compound C(Com C)存在的情况下,高氧+Gal-1+Com C组Nfr2的表达水平显著低于高氧+Gal-1组(P<0.05)。结论:Gal-1通过抑制炎症反应和氧化应激对高氧诱导的 ALI 发挥保护作用,这可能是通过激活 AMPK磷酸化而增强Nrf2通路实现的。
Abstract:
Objective:To observe the protective effect of galectin-1(Gal-1)on hyperoxia-induced acute lung injury(ALI)in neonatal rats,and to investigate its possible mechanism.Methods:30 neonatal Wistar rats were randomly divided into control group,hyperoxia group and hyperoxia+Gal-1 group,with 10 rats in each group.The rats in the control group breathed atmospheric air freely.The rats in the hyperoxia group and the hyperoxia+Gal-1 group were placed in a hyperoxia box,and the rats in the hyperoxia+Gal-1 group were injected 3 μg Gal-1 solution intraperitoneally 1 hour before being placed in the hyperoxia box.Rats in each group were sacrificed 12 hours after the start of the experiment,and samples were taken for analysis.After HE staining,the morphology of lung tissue was observed under an optical microscope.The lung tissue was taken and the dry-wet ratio(W/D)was calculated.Bronchoalveolar lavage fluid(BALF)was collected to detect the expression levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6).Part of lung tissue was taken,the expression levels of reactive oxygen species(ROS),superoxide dismutase(SOD)and malondialdehyde(MDA)were detected; RT-PCR was used to detect the expression levels of nuclear factor E2 related factor 2(Nrf2),heme oxygenase-1(HO-1),quinone oxidoreductase-1(NQO-1)mRNA; Western blot was used to detect the expression of related proteins.Results:Compared with the hyperoxia group,there was a small amount of fibrous exudation or inflammatory cell infiltration in the hyperoxia+Gal-1 group,and the degree of alveolar damage was between the control group and the hyperoxia group.The lung W/D value of rats in the hyperoxia group was significantly higher than that of the control group,while the W/D value of rats in the hyperoxia+Gal-1 group was lower than that of the hyperoxia group(all P<0.05).The expression levels of TNF-α,IL-1β and IL-6 in the BALF of rats in the hyperoxia group were significantly higher than those in the control group,and the expression levels of TNF-α,IL-1β and IL-6 in the rats in the hyperoxia+Gal-1 group were significantly lower than those of the hyperoxia group(all P<0.05).The expression levels of ROS and MDA in the lung tissue of rats in the hyperoxia group were significantly higher than those in the control group,and the expression level of SOD was significantly lower than that in the control group(all P<0.05); the expression levels of ROS and MDA in rats in the hyperoxia+Gal-1 group were significantly lower than those of the hyperoxia group,and the expression level of SOD was significantly higher than that of the hyperoxia group(all P<0.05).Compared with the control group and the hyperoxia group,the expression levels of Nrf2,HO-1 and NQO-1 mRNA in the lung tissue of rats in the hyperoxia+Gal-1 group were increased(all P<0.05).The pAMPK/AMPK in the hyperoxia+Gal-1 group was significantly higher than that in the control and hyperoxia groups(both P<0.05).The expression level of Nfr2 in the hyperoxia+Gal-1 group was significantly higher than that of the hyperoxia group(P<0.05); and in the presence of the AMPK inhibitor Compound C(Com C),the expression level of Nfr2 in the hyperoxia+Gal-1+Com C group was significantly lower than that of the hyperoxia+Gal-1 group(P<0.05).Conclusion:Gal-1 exerted protective effect against hyperoxia-induced ALI by inhibiting inflammatory response and oxidative stress,which was probably through the enhancement of Nrf2 pathway via activation of AMPK phosphorylation.

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备注/Memo

备注/Memo:
基金项目:陕西省重点研发计划项目(2017ZDXM-SF-020)
更新日期/Last Update: 2021-12-07