Protective effects of methane-rich saline on mice with allergic asthma by inhibiting inflammatory response, oxidative stress and apoptosis
Protective effects of methane-rich saline on mice with allergic asthma by inhibiting inflammatory response, oxidative stress and apoptosis
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DOI：
10.1631/jzus.b1900195
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发表时间：
2019-09
影响因子：
5.1
通讯作者：
Ning Zhang;Hong-tao Lu;Rong-jia Zhang;Xue-jun Sun
中科院分区：
文献类型：
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作者：
Ning Zhang;Hong-tao Lu;Rong-jia Zhang;Xue-jun Sun
哮喘是儿童和成人呼吸困难的常见原因，其特征是慢性气道炎症，可用治疗方法控制不佳。这导致严重残疾，给公共卫生系统带来巨大负担。甲烷已被证明是许多疾病的治疗剂。本研究旨在探讨富甲烷盐水（MRS）对哮喘小鼠病理生理的影响及其机制。本研究采用卵清蛋白（OVA）诱导的小鼠过敏性哮喘模型。将小鼠分为三组：对照组、OVA组和用MRS治疗的OVA诱导的哮喘小鼠作为第三组。测定肺阻力指数（RI）和动态顺应性（Cdyn），以确定气道高反应性（AHR）。进行苏木精和伊红（H&E）染色并评分以显示组织病理学变化。记录支气管肺泡灌洗液（BALF）细胞计数。采用酶联免疫吸附试验（ELISA）检测BALF和血清中细胞因子白细胞介素（IL）-4、IL-5、IL-13、肿瘤坏死因子α（TNF-α）和C-X-C基序趋化因子配体15（CXCL 15）的水平。采用商品化试剂盒测定氧化应激指标，包括丙二醛（MDA）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）、髓过氧化物酶（MPO）和8-羟基脱氧鸟苷（8-OHdG）。通过蛋白质印迹、实时定量聚合酶链反应（qRT-PCR）和生化检查评估细胞凋亡。MRS可逆转OVA诱导的AHR，减轻病理性炎症浸润，降低血清和BALF中细胞因子IL-4、IL-5、IL-13、TNF-α和CXCL 15的水平。此外，MRS给药后，氧化应激得到缓解，表现为MDA、MPO和8-OHdG降低，SOD和GSH升高。此外，MRS在该模型中表现出抗凋亡作用，保护上皮细胞免受损伤。甲烷改善过敏性哮喘小鼠模型的肺功能并减少浸润的炎性细胞。这可能与其抗炎、抗氧化和抗凋亡特性有关。
Asthma is a common cause of breathing difficulty in children and adults, and is characterized by chronic airway inflammation that is poorly controlled by available treatments. This results in severe disability and applies a huge burden to the public health system. Methane has been demonstrated to function as a therapeutic agent in many diseases. The aim of the present study was to explore the effect of methane-rich saline (MRS) on the pathophysiology of a mouse model of asthma and its underlying mechanism. A murine model of ovalbumin (OVA)-induced allergic asthma was applied in this study. Mice were divided into three groups: a control group, an OVA group, and OVA-induced asthmatic mice treated with MRS as the third group. Lung resistance index (RI) and dynamic compliance (Cdyn) were measured to determine airway hyper-responsiveness (AHR). Haematoxylin and eosin (H&E) staining was performed and scored to show histopathological changes. Cell counts of bronchoalveolar lavage fluid (BALF) were recorded. Cytokines interleukin (IL)-4, IL-5, IL-13, tumor necrosis factor α (TNF-α), and C-X-C motif chemokine ligand 15 (CXCL15) from BALF and serum were measured by enzyme-linked immunosorbent assay (ELISA). The oxidative stress indexes, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), myeloperoxidase (MPO), and 8-hydroxydeoxyguanosine (8-OHdG), were determined using commercial kits. Apoptosis was evaluated by western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and biochemical examination. MRS administration reversed the OVA-induced AHR, attenuated the pathological inflammatory infiltration, and decreased the cytokines IL-4, IL-5, IL-13, TNF-α, and CXCL15 in serum and BALF. Moreover, following MRS administration, the oxidative stress was alleviated as indicated by decreased MDA, MPO, and 8-OHdG, and elevated SOD and GSH. In addition, MRS exhibited an anti-apoptotic effect in this model, protecting epithelial cells from damage. Methane improves pulmonary function and decreases infiltrative inflammatory cells in the allergic asthmatic mouse model. This may be associated with its anti-inflammatory, antioxidative, and anti-apoptotic properties.