原儿茶酸对脂多糖诱导的急性肺损伤小鼠的保护作用  

Protective Effects of Protocatechuic Acid on Acute Lung Injury Induced by Lipopolysaccharide in Mice

作　　者：李君[1] 赵铭山[1] 张秀丽[2] 李岩[1] 韩冰[1] 

机构地区：[1]滨州医学院附属医院,山东滨州256603 [2]滨州医学院,山东烟台264003

出　　处：《现代生物医学进展》2014年第14期2646-2649,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81102828;81273037);山东省自然科学基金(Y2007C162)

摘　　要：目的:探索原儿茶酸(protocatechuicacid,PCA)对脂多糖(lipopolysaccharide,LPS)诱导的急性肺损伤(acute lung injury,ALI)小鼠的保护作用,探讨其保护机制。方法:将40只昆明小鼠按随机数字表法均分为空白对照组(NC组)、LPS模型组、原儿茶酸预处理组(PCA+LPS组)、地塞米松阳性对照组(Dex+LPS组),每组10只,模型组以5mg·kg-1脂多糖腹腔内注射诱导急性肺损伤。6h后处死小鼠,HE染色观察肺组织病理学变化;BCA法检测肺泡灌洗液中总蛋白浓度;ELISA检测肺泡灌洗液炎症因子TNF-α、IL-1β含量;Western Blot检测肺组织中p38MAPK、p-p38MAPK、p-ATF2蛋白的表达水平。结果:与对照组相比,模型组小鼠肺损伤明显,肺泡内出血、水肿、炎细胞浸润,肺泡灌洗液中TNF-α、IL-1β的含量及总蛋白浓度增加,肺组织中p38MAPK/p-p38MAPK、p-ATF2表达均明显增加(均P<0.01)。与模型组相比,原儿茶酸预处理组、地塞米松阳性对照组肺组织病理损伤程度明显减轻,肺泡灌洗液中TNF-α、IL-1β的含量及总蛋白浓度、肺组织中p38MAPK/p-p38MAPK、p-ATF2表达均明显降低(均P<0.01)。结论:PCA对LPS诱导的急性肺损伤有保护作用,其作用机制可能与其抑制p38MAPK-p-ATF2信号通路的活化、降低肺组织炎症反应有关。Objective： To investigate the protective effect of PCA on lung tissues during ALI in mice caused of by LPS and its possible mechanism. Methods： Forty Kunming mice were randomly divided into four groups： normal control group, LPS group, PCA pretreatment group（PCA＋LPS group）, dexamethasone positive control group（Dex＋LPS group） with ten mice in each group. ALI was induced by intraperitoneal injection of 5mg·kg-1 LPS. Mice were sacrificed at 6 hours, the lungs were harvested for observation of pathological changes. The total protein concentration in the bronchoalveolar lavage fluid were observed by BCA method and the levels of TNF-α and IL-1β in serum of BALF were tested by ELISA. The expression of p38MAPK, p-p38MAPK, p-ATF2 in lung tissue activation were detected by Western Blotting. Results： Compared with the control group, in the model group, there were significant lung structural damage, the histological results showed pulmonary alveolar hemorrhage, edema and inflammatory cell infiltration; the expression of TNF-α, IL-1β and the total protein concentration in BALF and the expression of p38MAPK/p-p38MAPK, p-ATF2 in lung tissue were significantly increased,（all P〈0.01）. Compared with the modal group, the lung histological changes were much more ameliorated, and the expression of TNF-α, IL-1β and the total protein concentration in BALF and the expression of p38MAPK/p-p38MAPK, p-ATF2 in lung tissue were markedly suppressed in PCA pretreatment group and dexamethasone positive control group（all P〈0.01）. Conclusion： PCA has remarkable protective effect on ALI induced by LPS in mice,its mechanism is possibly related to the inhibition p38MAPKp-ATF2 activation and reduction of inflammatory response in the lung tissue.

关 键 词：急性肺损伤 原儿茶酸 P38MAPK p-ATF2 

分 类 号：Q95-3[生物学—动物学] R563[医药卫生—呼吸系统]