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阿奇霉素对新生大鼠支气管肺发育不良的改善作用及机制
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| 篇名： | 阿奇霉素对新生大鼠支气管肺发育不良的改善作用及机制 |
| TITLE： | Improvement effects of azithromycin on bronchopulmonary dysplasia in neonatal rats and its mechanism |
| 摘要： | 目的 基于缺氧诱导因子1α（HIF-1α）/HIF-2α/血管内皮生长因子（VEGF）信号通路探讨阿奇霉素对新生大鼠支气管肺发育不良（BPD）的改善作用及机制。方法将60只新生SD大鼠随机分为阴性对照（NC）组、BPD组、阿奇霉素组、布地奈德组（阳性对照），每组15只。NC组大鼠正常呼吸空气，其余3组大鼠通过在高浓度氧中暴露14d构建BPD大鼠模型。建模成功后，阿奇霉素组大鼠腹腔注射阿奇霉素200mg/kg，布地奈德组大鼠雾化吸入布地奈德1.5mg/kg，每日1次，连续14d；BPD组和NC组大鼠不做任何处理。观察并检测各组大鼠肺组织病理学变化、放射状肺泡计数、肺泡平均截距，支气管肺泡灌洗液（BALF）中白细胞计数和肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、IL-1β、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、丙二醛（MDA）水平，肺组织中VEGF、HIF-1α、HIF-2αmRNA相对表达量和蛋白表达量。结果与NC组比较，BPD组大鼠肺组织出现明显损伤；白细胞计数、肺泡平均截距和TNF-α、IL-6、IL-1β、MDA水平均显著上调；放射状肺泡计数，SOD、CAT水平，VEGF、HIF-1α、HIF-2αmRNA相对表达量和蛋白表达量均显著下调（P＜0.05）。与BPD组比较，阿奇霉素组和布地奈德组大鼠上述指标均显著逆转（P＜0.05）。结论阿奇霉素可明显改善新生大鼠BPD的不良症状，抑制炎症及氧化应激反应，其作用机制可能是通过激活HIF-1α/HIF-2α/VEGF信号通路来实现肺保护作用。 |
| ABSTRACT： | OBJECTIVE To investigate the improvement effects of azithromycin on bronchopulmonary dysplasia （BPD） in neonatal rats based on hypoxia-inducible factor-1α（HIF-1α）/HIF-2α/vascular endothelial growth factor （VEGF） pathway. METHODS Sixty newborn SD rats were randomly divided into negative control group （NC）， BPD group， azithromycin group and budesonide group （positive control）， with 15 rats in each group. Rats in NC group were given normal breathing air， while rats in other three groups were exposed to high-concentration oxygen for 14 days to establish BPD rat models. After successful modeling， rats in azithromycin group were intraperitoneally injected with azithromycin 200 mg/kg， and rats in budesonide group were atomized with budesonide 1.5 mg/kg once a day for 14 consecutive days， while rats in BPD group and NC group were not treated. Pathological changes of lung tissue， radial alveolar count and mean alveolar intercept of rats were observed in each group. The white blood cell count in bronchoalveolar lavage fluid （BALF） and the levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， IL-1β， superoxide dismutase （SOD）， catalase （CAT） and malondialdehyde （MDA） were detected； mRNA and protein expressions of VEGF， HIF-1α， HIF-2α were also detected. RESULTS Compared with NC group， the lung tissue in BPD group was obviously damaged； the white blood cell count， average alveolar intercept and the levels of TNF-α， IL-6， IL-1β and MDA were significantly increased； the radial alveolar count， SOD and CAT levels， the relative expressions of VEGF， HIF-1α， HIF-2α mRNA and protein were significantly decreased （P＜0.05）. Compared with BPD group， the changes of the above indexes in azithromycin group and budesonide group were significantly reversed （P＜0.05）. CONCLUSIONS Azithromycin can obviously improve the symptoms of BPD in rats， reduce inflammation and oxidative stress， and exert lung protection， the mechanism of which may be realized by activating HIF-1α/HIF-2α/VEGF pathway. |
| 期刊： | 2024年第35卷第02期 |
| 作者： | 杜维纳；高淑强；巨容；习玉峰 |
| AUTHORS： | DU Weina，GAO Shuqiang，JU Rong，XI Yufeng |
| 关键字： | 阿奇霉素；支气管肺发育不良；氧化应激；免疫调节；缺氧诱导因子；血管内皮生长因子 |
| KEYWORDS： | azithromycin； bronchopulmonary dysplasia； |
| 阅读数： | 150 次 |
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