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Methane attenuates lung ischemia-reperfusion injury via regulating PI3K-AKT-NFκB signaling pathway
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-02-21 , DOI: 10.1080/10799893.2020.1727925
Fang Wang 1 , Feidi Wang 2 , Fengtao Li 1 , Dong Wang 1 , Haopeng Li 1 , Xijing He 1 , Jingyao Zhang 3
Affiliation  

Abstract Objective: This study aims to investigate the protective effects and possible mechanism of methane-rich saline (MS) on lung ischemia-reperfusion injury (LIRI) in rats. Methods: MS (2 ml/kg and 20 ml/kg) was injected intraperitoneally in rats after LIRI. Lung injury was assayed by Hematoxylin-eosin (HE) staining and wet-to-dry weight (W/D). The cells in the bronchoalveolar lavage fluid (BALF) and blood were counted. Oxidative stress was examined by the level of malondialdehyde (MDA) and superoxide dismutase (SOD). Inflammatory factors including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were determined by ELISA. Lung tissue apoptosis was detected by TUNEL staining and western blotting of Bcl-2, Bax, and caspase-3. The expressions of IкBα, p38, PI3K, AKT, and NF-κB were analyzed with Western blotting. Results: MS effectively decreased the lung W/D ratio as well as the lung pathological damage and reduced the localized infiltration of inflammatory cells. Methane suppressed the expression of the PI3K-AKT-NFκB signaling pathway during the lung IR injury, which inhibited the activation of NF-kB and decreased the level of inflammatory cytokines, such as TNF-α, IL-1β, and IL-10. Moreover, we found that MS treatment relieved reactive oxygen species (ROS) damage by downregulating MDA and upregulating SOD. MS treatment also regulated apoptosis-related proteins, such as Bcl-2, Bax, and caspase-3. Conclusions: MS could repair LIRI and reduce the release of oxidative stress, inflammatory cytokines, and cell apoptosis via the PI3K-AKT-NFκB signaling pathway, which may provide a novel and promising strategy for the treatment of LIRI.

中文翻译:

甲烷通过调节PI3K-AKT-NFκB信号通路减轻肺缺血再灌注损伤

摘要 目的:本研究旨在探讨富甲烷盐水(MS)对大鼠肺缺血再灌注损伤(LIRI)的保护作用及其可能机制。方法:大鼠LIRI后腹腔注射MS(2 ml/kg和20 ml/kg)。通过苏木精-伊红 (HE) 染色和湿干重 (W/D) 测定肺损伤。对支气管肺泡灌洗液 (BALF) 和血液中的细胞进行计数。通过丙二醛 (MDA) 和超氧化物歧化酶 (SOD) 的水平检查氧化应激。炎症因子包括肿瘤坏死因子-α (TNF-α)、白介素-1β (IL-1β) 和白介素-10 (IL-10) 通过 ELISA 测定。通过 TUNEL 染色和 Bcl-2、Bax 和 caspase-3 的蛋白质印迹检测肺组织凋亡。用蛋白质印迹分析 IкBα、p38、PI3K、AKT 和 NF-κB 的表达。结果:MS有效降低肺W/D比值和肺病理损伤,减少炎症细胞的局部浸润。甲烷在肺 IR 损伤期间抑制 PI3K-AKT-NFκB 信号通路的表达,从而抑制 NF-kB 的激活并降低炎症细胞因子的水平,如 TNF-α、IL-1β 和 IL-10。此外,我们发现 MS 治疗通过下调 MDA 和上调 SOD 来减轻活性氧 (ROS) 损伤。MS 治疗还调节凋亡相关蛋白,如 Bcl-2、Bax 和 caspase-3。结论:MS可通过PI3K-AKT-NFκB信号通路修复LIRI,减少氧化应激、炎症细胞因子的释放和细胞凋亡,为LIRI的治疗提供一种新的、有前景的策略。MS有效降低肺W/D比值以及肺病理损伤,减少炎症细胞的局部浸润。甲烷在肺 IR 损伤期间抑制 PI3K-AKT-NFκB 信号通路的表达,从而抑制 NF-kB 的激活并降低炎症细胞因子的水平,如 TNF-α、IL-1β 和 IL-10。此外,我们发现 MS 治疗通过下调 MDA 和上调 SOD 来减轻活性氧 (ROS) 损伤。MS 治疗还调节凋亡相关蛋白,如 Bcl-2、Bax 和 caspase-3。结论:MS可通过PI3K-AKT-NFκB信号通路修复LIRI,减少氧化应激、炎症细胞因子的释放和细胞凋亡,为LIRI的治疗提供一种新的、有前景的策略。MS有效降低肺W/D比值以及肺病理损伤,减少炎症细胞的局部浸润。甲烷在肺 IR 损伤期间抑制 PI3K-AKT-NFκB 信号通路的表达,从而抑制 NF-kB 的激活并降低炎症细胞因子的水平,如 TNF-α、IL-1β 和 IL-10。此外,我们发现 MS 治疗通过下调 MDA 和上调 SOD 来减轻活性氧 (ROS) 损伤。MS 治疗还调节凋亡相关蛋白,如 Bcl-2、Bax 和 caspase-3。结论:MS可通过PI3K-AKT-NFκB信号通路修复LIRI,减少氧化应激、炎症细胞因子的释放和细胞凋亡,为LIRI的治疗提供一种新的、有前景的策略。
更新日期:2020-02-21
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