ABSTRACT

Asthma is one of the most common respiratory diseases in the world. Nevertheless, it is reported that inflammation induced by asthma is not only restricted to the lung and may cause damaging effects on remote organs. Therefore, this study was designed to investigate the beneficial effects of long-term sodium hydrosulfide (NaHS) administration on lung inflammation and oxidative stress markers to protect the kidney during chronic asthma. BALB/c mice were divided into three groups (n = 5–7): control, asthma and NaHS. Except the control group, sensitization and challenge were performed with ovalbumin. The NaHS group intraperitoneally received 14 μmol/kg NaHS 30 min before each challenge. 24 h after the last challenge, samples of bronchoalveolar lavage fluid (BALF), plasma, lung and kidney tissues were collected. NaHS administration significantly decreased total white blood cell count, percentages of eosinophils, neutrophils and macrophages and increased percentage of lymphocytes. Administration of NaHS considerably decreased the levels of BALF interleukin-13, plasma tumor necrosis factor-alpha (TNF-α), lung malondialdehyde (MDA) and lung phosphorylated nuclear factor-kappa B (p-NF-κB) expression and scores of peribronchial inflammatory cell infiltration, goblet cell hyperplasia and subepithelial fibrosis and increased the activity of lung superoxide dismutase (SOD). The MDA levels and expressions of p-ERK1/2 and Bax were decreased and SOD activity and expressions of Bcl-2 and p-Akt were significantly increased in kidney tissues by NaHS administration. Administration of NaHS decreased renal oxidative stress indices and reduced apoptosis by the inhibition of TNF-α/ERK1/2/Bax. Therefore, H₂S may have an essential role in renal protection during asthma.

摘要

哮喘是世界上最常见的呼吸道疾病之一。然而，据报道，哮喘引起的炎症不仅限于肺部，还可能对远处器官造成破坏性影响。因此，本研究旨在调查长期硫氢化钠 (NaHS) 给药对肺部炎症和氧化应激标志物的有益影响，从而在慢性哮喘期间保护肾脏。BALB/c小鼠分为三组（n= 5–7)：对照、哮喘和 NaHS。除对照组外，均用卵清蛋白进行致敏和激发。NaHS 组在每次攻击前 30 分钟腹腔内接受 14 μmol/kg NaHS。最后一次攻击后 24 小时，收集支气管肺泡灌洗液 (BALF)、血浆、肺和肾组织的样本。NaHS 给药显着降低了总白细胞计数、嗜酸性粒细胞、中性粒细胞和巨噬细胞的百分比，并增加了淋巴细胞的百分比。NaHS 显着降低了 BALF 白细胞介素 13、血浆肿瘤坏死因子-α (TNF-α)、肺丙二醛 (MDA) 和肺磷酸化核因子-κ B 的水平（p-NF-κB) 的表达和支气管周围炎性细胞浸润、杯状细胞增生和上皮下纤维化的评分以及肺超氧化物歧化酶 (SOD) 的活性增加。NaHS给药后肾组织中MDA水平和p -ERK1/2和Bax表达降低，SOD活性和Bcl-2和p -Akt表达显着增加。NaHS 的施用通过抑制 TNF-α/ERK1/2/Bax 降低了肾氧化应激指数并减少了细胞凋亡。因此，H ₂ S 可能在哮喘期间的肾脏保护中发挥重要作用。