Tang Shih-En, Liao Wen-I, Wu Shu-Yu, Pao Hsin-Ping, Huang Kun-Lun, Chu Shi-Jye
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan.
Front Physiol. 2020 Jan 31;10:1616. doi: 10.3389/fphys.2019.01616. eCollection 2019.
Previous investigations reveal that BTP2, a store-operated calcium channel blocker, has protective and anti-inflammatory properties in multiple inflammatory diseases. This study investigates whether BTP2 can protect against decompression sickness (DCS) in a rat model.
BTP2 (2 mg/kg) was administered to male Sprague-Dawley rats 30 min before subjecting them to hyperbaric pressure. Control rats were not treated. After decompression, signs of DCS were examined, and samples of bronchoalveolar lavage fluid and lung tissue were obtained for evaluation.
The incidence and mortality of DCS were decreased significantly in rats treated with BTP2 compared to those treated with dimethyl sulfoxide. BTP2 significantly attenuated DCS-induced lung edema, histological evidence of lung inflammation, necroptosis, and apoptosis, while it decreased levels of tumor necrosis factor alpha, interleukin-6, and cytokine-induced neutrophil chemoattractant-1 in bronchoalveolar lavage fluid. In addition, BTP2 reduced the expression of nuclear factor of activated T cells and early growth response protein 3 in lung tissue. BTP2 also significantly increased the levels of inhibitor kappa B alpha and suppressed the levels of nuclear factor kappa B in lung tissue.
The results suggest that BTP2 may has potential as a prophylactic therapy to attenuate DCS-induced injury.
先前的研究表明，BTP2作为一种储存式钙通道阻滞剂，在多种炎症性疾病中具有保护和抗炎特性。本研究旨在探讨BTP2是否能在大鼠模型中预防减压病（DCS）。
在对雄性Sprague-Dawley大鼠施加高压前30分钟，给予其BTP2（2毫克/千克）。对照组大鼠不进行处理。减压后，检查DCS的体征，并获取支气管肺泡灌洗液和肺组织样本进行评估。
与用二甲基亚砜处理的大鼠相比，用BTP2处理的大鼠中DCS的发病率和死亡率显著降低。BTP2显著减轻了DCS诱导的肺水肿、肺部炎症的组织学证据、坏死性凋亡和凋亡，同时降低了支气管肺泡灌洗液中肿瘤坏死因子α、白细胞介素-6和细胞因子诱导的中性粒细胞趋化因子-1的水平。此外，BTP2降低了肺组织中活化T细胞核因子和早期生长反应蛋白3的表达。BTP2还显著提高了肺组织中抑制蛋白κBα的水平，并抑制了核因子κB的水平。
结果表明，BTP2可能具有作为预防性治疗减轻DCS诱导损伤的潜力。
