Department of Anesthesiology, The Central Hospital of Huzhou, Huzhou, Zhejiang, China (mainland).
Department of Anesthesiology, Huzhou Municipal Women and Children's Health Center, Huzhou, Zhejiang, China (mainland).
Med Sci Monit. 2018 Jul 14;24:4869-4875. doi: 10.12659/MSM.908887.
BACKGROUND The purpose of this study was to investigate whether DEX exerts protective mechanisms in rats with acute lung injury (ALI) induced by the endotoxin lipopolysaccharide (LPS). The mortality rate of ALI is extremely high. DEX, an a2 adrenergic receptor agonist, has potent anti-inflammatory and organ-protective effects in addition to its sedative and analgesic properties. We sought to elucidate whether DEX can attenuate acute lung injury. MATERIAL AND METHODS Forty-eight Wister rats were randomly divided into 4 groups (n=12, per group): the normal saline control (NS) group, receiving tail-vein injection of 0.9% normal saline (5 mL/kg); the LPS (L) group, receiving tail-vein injection of LPS (8 mg/kg); the LPS+DEX (L+D) group, receiving tail-vein injection of LPS (8 mg/kg), 0.5h before treated with DEX (50 ug/kg); and the DEX+LPS (D+L) group, receiving tail-vein injection of LPS (8 mg/kg) 0.5 h after being treated with DEX (50 ug/kg). Then, we measured the wet‑to‑dry weight ratio of lung tissue, the ALI pathology score, and HE staining of lung tissue, and assessed the Oxygen Tension index. RESULTS The present study revealed that LPS‑induced rats exhibited significant lung injury, characterized by the deterioration of histopathology, ALI Pathology Score, wet‑to‑dry weight ratio, and Oxygen Tension index (MBP, PaO2, PaCO2, PH, HCO3-, and Lac), which were attenuated by DEX treatment. CONCLUSIONS Collectively, the present results demonstrate elucidate the molecular mechanisms by which DEX ameliorates LPS‑induced ALI.
本研究旨在探讨地塞米松(DEX)是否对脂多糖(LPS)诱导的急性肺损伤(ALI)大鼠发挥保护作用。ALI 的死亡率极高。DEX 作为一种 a2 肾上腺素能受体激动剂,除具有镇静和镇痛作用外,还具有强大的抗炎和器官保护作用。我们试图阐明 DEX 是否可以减轻急性肺损伤。
48 只 Wister 大鼠随机分为 4 组(每组 n=12):生理盐水对照组(NS),尾静脉注射 0.9%生理盐水(5 mL/kg);LPS 组(L),尾静脉注射 LPS(8 mg/kg);LPS+DEX 组(L+D),尾静脉注射 LPS(8 mg/kg)前 0.5 小时给予 DEX(50 ug/kg);DEX+LPS 组(D+L),尾静脉注射 LPS(8 mg/kg)后 0.5 小时给予 DEX(50 ug/kg)。然后,我们测量肺组织湿重与干重比、ALI 病理评分和肺组织 HE 染色,并评估氧分压指数。
本研究表明 LPS 诱导的大鼠表现出明显的肺损伤,其特征为组织病理学恶化、ALI 病理评分、湿重与干重比以及氧分压指数(MBP、PaO2、PaCO2、PH、HCO3-和 Lac)降低,DEX 治疗可减轻这些损伤。
综上所述,本研究结果阐明了 DEX 改善 LPS 诱导的 ALI 的分子机制。