艾司洛尔对脓毒症急性肺损伤大鼠肺泡炎症因子及氧化应激蛋白的调控研究

分析艾司洛尔对脓毒症急性肺损伤大鼠肺泡炎症因子及氧化应激蛋白的调控作用。将清洁级雄性SD大鼠随机分为4组,每组10只。对照组和模型组大鼠给予生理盐水1 mL/kg灌胃治疗,地塞米松组(地塞米松0.25 mg/kg)和艾司洛尔组(艾司洛尔5 mg/kg)大鼠给予相对应的药物灌胃,每日一次,连续6天。末次给药后对照组给予生理盐水尾静脉注射,其余各组给予内毒素(3 mg/kg)尾静脉注射造模。测定各组大鼠的肺功能,并检测各组大鼠肺泡中炎症因子及氧化应激蛋白水平变化。结果显示:与对照组相比,模型组大鼠的肺功能指标呼吸频率及肺泡通透指数均明显升高(P<0.05),血氧分压(PaO₂)明显降低(P<0.05),模型组大鼠的炎症因子白细胞介素2(IL-2)和IL-6、还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)及NOX4水平均明显升高(P<0.05)；而地塞米松组和艾司洛尔组的上述指标得到明显恢复(P<0.05),且艾司洛尔组恢复更明显(P<0.05)。因此,艾司洛尔能显著改善脓毒症急性肺损伤,可能与其调控大鼠肺泡炎症因子及氧化应激蛋白的水平有关。

Effects of esmolol on alveolar inflammatory factors and oxidative stress proteins in septic rats with acute lung injury

The aim of this study was to investigate the effects of esmolol on alveolar inflammatory factors and oxidative stress protein in septic rats with acute lung injury. Clean grade male SD rats were randomly divided into four groups (n=10). Rats in the control group and model group were given saline 1 ml/kg intragastric administration. The rats in dexamethasone group (0.25 mg/kg) and esmolol group (5 mg/kg) were given corresponding drugs by gavage. Once a day for 6 consecutive days. After the last administration, the control group was given tail vein injection of normal saline, and the other groups were given tail vein injection of endotoxin (3mg/kg) to establish the model. The pulmonary function of rats in each group was measured 24 hours later, and the levels of inflammatory factors and oxidative stress protein in alveoli of rats in each group were detected. The results showed that compared with the control group, the respiratory rate, and alveolar permeability index of pulmonary function in the model group were significantly higher (P<0.05). Inflammatory cytokines IL-2 and IL-6, NOX2 and NOX4 levels in the model group increased significantly (P<0.05). The above indexes of dexamethasone group and esmolol group were obviously restored (P<0.05). Esmolol group recovered more significantly (P<0.05). So Esmolol can significantly improve acute lung injury in sepsis rats, which may be related to its regulation of alveolar inflammatory factors and oxidative stress protein levels.