| 李君 赵铭山 张秀丽 李岩 韩冰.原儿茶酸对脂多糖诱导的急性肺损伤小鼠的保护作用[J].,2014,14(14):2646-2649 |
| 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 Inducedby Lipopolysaccharide in Mice |
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| DOI： |
| 中文关键词: 急性肺损伤 原儿茶酸 p38MAPK p-ATF2 |
| 英文关键词: ALI PCA p38MAPK p-ATF2 |
| 基金项目:国家自然科学基金项目（81102828；81273037）；山东省自然科学基金（Y2007C162） |
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| 中文摘要: |
| 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-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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