Division of Surgical Intensive Care Unit, Department of Surgery, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City, Taiwan.
Institute of Emergency and Critical Care Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Inflammation. 2017 Apr;40(2):555-565. doi: 10.1007/s10753-016-0502-4.
Inflammation following hemorrhagic shock/resuscitation (HS/RES) induces acute lung injury (ALI). Dimethyl sulfoxide (DMSO) possesses anti-inflammatory and antioxidative capacities. We sought to clarify whether DMSO could attenuate ALI induced by HS/RES. Male Sprague-Dawley rats were allocated to receive either a sham operation, sham plus DMSO, HS/RES, or HS/RES plus DMSO, and these were denoted as the Sham, Sham + DMSO, HS/RES, or HS/RES + DMSO group, respectively (n = 12 in each group). HS/RES was achieved by drawing blood to lower mean arterial pressure (40-45 mmHg for 60 min) followed by reinfusion with shed blood/saline mixtures. All rats received an intravenous injection of normal saline or DMSO immediately before resuscitation or at matching points relative to the sham groups. Arterial blood gas and histological assays (including histopathology, neutrophil infiltration, and lung water content) confirmed that HS/RES induced ALI. Significant increases in pulmonary expression of tumor necrosis factor-α (TNF-α), malondialdehyde, nuclear factor-kappa B (NF-κB), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX-2) confirmed that HS/RES induced pulmonary inflammation and oxidative stress. DMSO significantly attenuated the pulmonary inflammation and ALI induced by HS/RES. The mechanisms for this may involve reducing inflammation and oxidative stress through inhibition of pulmonary NF-κB, TNF-α, iNOS, and COX-2 expression.
出血性休克/复苏（HS/RES）后炎症会引起急性肺损伤（ALI）。二甲基亚砜（DMSO）具有抗炎和抗氧化作用。我们旨在阐明 DMSO 是否可以减轻 HS/RES 引起的 ALI。雄性 Sprague-Dawley 大鼠被分为接受假手术、假手术加 DMSO、HS/RES 或 HS/RES 加 DMSO，分别记为 Sham、Sham+DMSO、HS/RES 和 HS/RES+DMSO 组（每组 n=12）。HS/RES 通过抽血将平均动脉压降低（40-45mmHg 持续 60min），然后再输入放血/盐水混合物进行再灌注。所有大鼠在复苏前或相对于 Sham 组的匹配点立即接受生理盐水或 DMSO 静脉注射。动脉血气和组织学检测（包括组织病理学、中性粒细胞浸润和肺水含量）证实 HS/RES 引起 ALI。肿瘤坏死因子-α（TNF-α）、丙二醛、核因子-κB（NF-κB）、诱导型一氧化氮合酶（iNOS）和环氧化酶 2（COX-2）在肺部的表达显著增加，证实 HS/RES 引起肺部炎症和氧化应激。DMSO 显著减轻 HS/RES 引起的肺部炎症和 ALI。其机制可能涉及通过抑制肺 NF-κB、TNF-α、iNOS 和 COX-2 的表达来减轻炎症和氧化应激。
