红景天苷注射液对脂多糖诱导脓毒性休克肺损伤大鼠肺血管通透性的影响

目的:探讨红景天苷注射液对脂多糖诱导脓毒性休克肺损伤大鼠肺血管通透性的影响。方法:75只SD大鼠随机分为对照组、模型组、阳性对照组、Sal-L组、Sal-H组，对照组不予任何处理，模型组通过脂多糖造模，阳性对照组造模后给予5 mg/kg地塞米松，Sal-L组、Sal-H组造模后分别给予0.68、1.09 ng/kg红景天苷注射液，比较各组肺组织病理学、肺损伤评分（LIS）、肺湿/干质量比（W/D）、肺通透指数（LPI）、肺组织中伊文思蓝含量、氧化应激指标［髓过氧化物酶活性（MPO）、丙二醛（MDA）、超氧化物岐化酶（SOD）］、炎症指标［白介素（IL）-1、IL-6、肿瘤坏死因子-α（TNF-α）、核因子κB（NF-κB）、磷酸化NF-κB p65（p-NF-κB p65）、NF-κB抑制蛋白IκBa磷酸化蛋白（p-IκBa）］表达。结果:对照组双肺无异常；模型组大鼠一般情况、肺部出现明显病理变化，阳性对照组、Sal-L组、Sal-H组较模型组不同程度改善。与模型组相比，Sal-L组、Sal-H组LIS、W/D、LPI呈剂量依赖性降低（P＜0.05）。与模型组相比，Sal-L组、Sal-H组肺组织中伊文思蓝含量呈剂量依赖性降低（P＜0.05）。与模型组相比，Sal-L组、Sal-H组MPO、MDA呈剂量依赖性降低，SOD呈剂量依赖性升高（P＜0.05）。与模型组相比，Sal-L组、Sal-H组IL-1、IL-6、TNF-α、NF-κB mRNA及p-NF-κB p65、p-IκBa蛋白呈剂量依赖性降低（P＜0.05）。结论:红景天苷注射液可改善脓毒症休克肺损伤大鼠肺血管通透性，减轻肺水肿，其机制可能与抗氧化应激，抑制炎症反应有关。

Effects of salidroside injection on pulmonary vascular permeability in rats with septic shock induced lung injury induced by lipopolysaccharide

AIM: To investigate the effects of salidroside injection on pulmonary vascular permeability in rats with septic shock induced lung injury induced by lipopolysaccharide. METHODS: Seventy-five Sprague-Dawley rats were randomly divided into control group, model group, positive control group, Sal-L group and Sal-H group. The control group did not receive any treatment. The model group was modeled by lipopolysaccharide, and the positive control group was modeled. After administration of 5 mg/kg dexamethasone, Sal-L group and Sal-H group were given 0.68 and 1.09 ng/kg salidroside injection, respectively. The lung histopathology and lung injury score (LIS) were compared, as well as lung wet/dry mass ratio (W/D), lung permeability index (LPI), Evans blue content in lung tissue, oxidative stress index ［myeloperoxidase activity (MPO), malondialdehyde (MDA) , superoxide dismutase (SOD)］, inflammation indicators ［interleukin (IL)-1, IL-6, tumor necrosis factor-α (TNF-α), nuclear factor κB (NF-κB), phosphorylated NF-κB p65 (p-NF-κB p65), NF-κB inhibitor protein IκBa phosphorylated protein (p-IκBa)］ expression. RESULTS:There were no abnormalities in the lungs of the control group; the general condition and the pathological changes in the lungs were observed in the model group, and the positive control group, the Sal-L group and the Sal-H group were improved to some extents compared with the model group. Compared with the model group, the LIS, W/D, and LPI in the Sal-L group and the Sal-H group were decreased in a dose-dependent manner (P＜0.05). Compared with the model group, the content of Evans blue in the tissue in Sal-L group and Sal-H group decreased in a dose-dependent manner (P＜0.05). Compared with the model group, the MPO and MDA in the Sal-L group and the Sal-H group decreased in a dose-dependent manner, and the SOD was dose-dependently elevated (P＜0.05). Compared with the model group, IL-1, IL-6, TNF-α, NF-κB mRNA and p-NF-κB p65, p-IκBa protein in Sal-L group and Sal-H group was decreased in a dose-dependent manner (P＜0.05). CONCLUSION: Salidroside injection can improve pulmonary vascular permeability and reduce pulmonary edema in rats with septic shock and lung injury. The mechanism may be related to anti-oxidative stress and inhibition of inflammatory response.