Substance P attenuates hyperoxia‑induced lung injury in neonatal rats.
Substance P attenuates hyperoxia‑induced lung injury in neonatal rats.
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DOI：
10.3892/mmr.2013.1809
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发表时间：
2014-02
影响因子：
3.4
通讯作者：
Lin Yang;Cong Liu;H. Dang;F. Fang;Lingping Tan;P. Zhao;Feng Xu;Chenjun Liu
中科院分区：
文献类型：
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作者：
Lin Yang;Cong Liu;H. Dang;F. Fang;Lingping Tan;P. Zhao;Feng Xu;Chenjun Liu
本研究旨在探讨P物质(SP)在新生大鼠高氧性肺损伤中的作用，并探讨其通过声波刺激物(SHH)信号通路的保护作用机制。12小时龄新生SD大鼠随机分为空气组、高氧组、空气+SP组和高氧+SP组。在另一组单独的实验中，新生大鼠幼鼠暴露在21或95%O2中14天，无论有没有腹腔注射SP。分别于高氧暴露第3、7、14天处死动物。光镜下观察肺组织病理改变及肺组织损伤程度。用丙二醛(MDA)评价氧化应激，用超氧化物歧化酶(SOD)测定组织匀浆的抗氧化活性。用定量聚合酶链式反应(QPCR)和免疫印迹分析检测SHH基因和蛋白的表达。高氧组出现明显的急性肺损伤(ALI)特征。与单纯高氧治疗相比，加用SP后肺损伤明显减轻。此外，加入SP后，丙二醛水平显著降低，超氧化物歧化酶水平显著升高。SP刺激可能导致SHH信号通路的激活，经SP处理后SHH的表达明显增加。本研究表明，SP对高氧性肺损伤具有保护作用，其机制可能与减轻氧化应激、提高抗氧化剂活性、上调SHH信号转导通路有关。
The aim of the study was to investigate the effects of substance P (SP) in hyperoxia‑induced lung injury in newborn rats and to elucidate its protective mechanism of action via the sonic hedgehog (SHH) signaling pathway. Twelve‑hour‑old neonatal Sprague‑Dawley rats were randomly divided into one of four groups: air, hyperoxia, air + SP and hyperoxia + SP. In a separate set of experiments, the neonatal rat pups were exposed to 21 or 95% O2 for 14 days with or without intraperitoneal administration of rat SP. The animals were sacrificed at 3, 7 and 14 days, respectively, of hyperoxia exposure. Lung pathology and grade of lung tissue injury were examined by light microscopy. Oxidative stress was evaluated by malondialdehyde (MDA) and antioxidant activity was measured by superoxide dismutase (SOD) in tissue homogenates. The expression of SHH mRNA and protein were detected by quantitative polymerase chain reaction (qPCR) and western blot analysis, respectively. In the hyperoxia group, marked characteristics of acute lung injury (ALI) were observed. Compared with the simple hyperoxia treatment, the lung damage was significantly ameliorated following the addition of SP. Furthermore, the levels of MDA were decreased and SOD was significantly increased following the addition of SP. SP stimulation may result in activation of the SHH signaling pathway and the expression of SHH markedly increased following treatment with SP. The present study demonstrated that SP protected against the hyperoxia‑induced lung damage by attenuating oxidative stress, elevating the antioxidant activities and upregulating the signaling pathway of SHH.