红景天苷对氯气暴露致急性肺损伤肺血管通透性的保护作用

目的：观察红景天苷对氯气暴露致大鼠急性肺损伤肺血管通透性的干预作用，探讨其改善肺损伤的可能作用机制。方法：40只SD大鼠随机分为4组，分别为阴性对照组、氯气暴露组、红景天苷干预组和单纯红景天苷组。阴性对照组和单纯红景天苷组以空气为对照，氯气暴露组和红景天苷干预组给予1 200 mg/m³氯气动态染毒，染毒时间为5 min；红景天苷干预组和单纯红景天苷组在氯气染毒前30 min和染毒后15 min分两次给予300 mg/kg红景天苷灌胃，阴性对照组和氯气暴露组予以等量生理盐水灌胃。常规苏木精-伊红染色法（HE）染色后观察大鼠肺损伤的程度；二辛可宁酸（BCA）蛋白定量法测定血浆和支气管肺泡灌注液（BALF）中蛋白含量并计算肺血管通透指数；肺组织冰冻切片采用二氢乙啶（DHE）探针检测肺组织活性氧（ROS）的含量；试剂盒检测BALF中丙二醛（MDA）、氧化型谷胱甘肽（GSSG）和还原型谷胱甘肽（GSH）的含量以及超氧化物歧化酶（SOD）的活力；Western blot法检测肺组织中SOD2的表达。结果：氯气暴露后3 h观察，与阴性对照组比较，氯气暴露组肺组织可见大鼠支气管柱状上皮损伤、肺泡结构破坏以及肺间隔轻度炎细胞浸润，BALF中SOD活力升高，差异有统计学意义（P<0.05）；与氯气暴露组比较，红景天苷可升高BALF中GSH含量，降低因氯气暴露引起的肺组织ROS水平和BALF中MDA和GSSG含量（P<0.05），下调肺组织中SOD2蛋白的表达水平（P<0.05）。结论：红景天苷可能通过降低肺内氧化应激水平，改善氯气暴露引起的急性肺损伤。

Protective effects of salidroside on chlorine-induced acute lung injury in rats

OBJECTIVE: To investigate the protective effects of salidroside on acute lung injury (ALI) in rats which were exposed to chlorine,and to explore the protective mechanism. METHODS: Fortymale Sprague-Dawley (SD) rats were randomly divided into four groups:control,chlorine,chlorine+salidroside and salidroside. Chlorine and chlorine+salidroside groups were exposed to chlorine of 1 200 mg/m³ for 5 minutes. Chlorine+salidroside and salidroside groups were treated with salidroside (300 mg/kg) at 30 minutes before chlorineexposure and at 15 minutes after chlorine exposure. At 3 hours after chlorine exposure,histopathological analysis was conducted to evaluate the degree of ALI and dihydroethidium (DHE) assay was used to determine the level of pulmonary reactive oxygen species (ROS). Lung permeation index was calculated by protein detecting. The malondialdehyde (MDA),superoxide dismutase (SOD),L-glutathione (GSH) and oxidized glutathione (GSSG) in BALF were measured by kits. The protein level of SOD1 and SOD2 were detected by western blotting. RESULTS: At 3 hours after chlorine exposure,there appeared marked histopathological changes in the lung,including macrophage and neutrophile granulocyte infiltration and edema emerging in bronchiolar and pulmonary alveolar. The ROS level in lung and the lung permeation index were higher. MDA, SOD,GSSG of BALF increased significantly (P<0.05) compared with control group. The GSH and GSH/GSSG ratio in BALF were lower than that in the control group (P<0.05). SOD activity in BALF,and SOD1 and SOD2 protein expression were significantly elevated in chlorine group. In the chlorine+salidroside group,the lung permeation index,ROS level in the lung,MDA and GSSG in BALF decreased significantly (P<0.05) compared with the chlorine group. The GSH/GSSG ratio in BALF were higher than that in the chlorine group (P<0.05). SOD1 and SOD2 protein expression were significantly reduced (P<0.05). CONCLUSION: Our data show that chlorine exposure induced ALI. Administration of salidroside reduce the chlorine-induced ALI via reduction of oxidative stress.