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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-琢、IL-1茁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。

英文摘要:

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-αand IL-1βin serum of BALF were tested by ELISA. The expression of p38MAPK, p-p38MAPK, p-ATF2 in lung tissue activation were detected by Western Blotting.Result: 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-1βand 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-1βand 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.

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