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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 explore the protective effect of protocatechuic acid (PCA) on lipopolysaccharide (LPS) -induced acute lung injury (ALI) in mice and its protective mechanism. Methods: 40 Kunming mice were randomly divided into control group (NC group), LPS model group, protocatechuic acid pretreatment group (PCA + LPS group), dexamethasone positive control group (Dex + LPS group), 10 rats in each group. The acute lung injury was induced by intraperitoneal injection of 5 mg · kg-1 lipopolysaccharide in model group. Six hours later, the mice were sacrificed and the pathological changes of lung were observed by HE staining. The total protein concentration in BALF was measured by BCA method. The levels of TNF-α and IL-1β in bronchoalveolar lavage fluid were detected by ELISA. p38MAPK, p-p38MAPK, p-ATF2 protein expression levels. Results: Compared with the control group, the lung injury in the model group was obvious. The contents of TNF-α, IL-1β and total protein in the alveolar hemorrhage, edema and inflammatory cell infiltration, p-p38MAPK, p-ATF2 expression were significantly increased (all P <0.01). Compared with the model group, the degree of pathological damage of lung tissue in protocatechuic acid pretreatment group and dexamethasone positive control group was significantly reduced. The contents of TNF-α, IL-1β and total protein in bronchoalveolar lavage fluid in lung tissue The expressions of p38MAPK / p-p38MAPK and p-ATF2 were significantly decreased (all P <0.01). CONCLUSION: PCA can protect LPS-induced acute lung injury and its mechanism may be related to the inhibition of p38 MAPK-p-ATF2 signaling pathway and the reduction of lung inflammation.