Ma Quanxin, Wang Kai, Yang Qinqin, Ping Shun, Zhao Weichun, Shou Qiyang, Zhou Weimin, Chen Minli
Animal Experimental Research Center, Zhejiang Chinese Medical University, Hangzhou 310053, China.
College of Animal Sciences, Zhejiang University, Hangzhou 310058, China; Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, China.
Mediators Inflamm. 2016;2016:7934049. doi: 10.1155/2016/7934049. Epub 2016 Nov 6.
is a traditional medical plant in China which is widely used in folk medicine due to its versatile biological activities, especially for its anti-inflammatory effects. However, the detailed mechanism underlying this action is not clear. Here, we studied the protective effects of against acute lung injury (ALI), and we further explored the pharmacological mechanisms of this action. We found that pretreatment with suppressed the release of proinflammatory cytokines in the serum of ALI mice. Histological analysis of lung tissue demonstrated that inhibited LPS-induced lung injury, improved lung morphology, and reduced the activation of nuclear factor-B (NF-B) in the lungs. Furthermore, the anti-inflammatory actions of were investigated . We observed that suppressed the mRNA expression of interleukin-1 (IL-1), IL-6, monocyte chemotactic protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and tumor necrosis factor- (TNF-) in RAW264.7 cells challenged with LPS. Furthermore, pretreatment of reduced the phosphorylation of p65 and IB- which is activated by LPS. In conclusion, our data firstly demonstrated that the anti-inflammatory effects of against ALI were achieved through downregulation of the NF-B signaling pathway, thereby reducing the production of inflammatory mediators.
是中国的一种传统药用植物，因其具有多种生物活性，特别是抗炎作用，而在民间医学中被广泛应用。然而，这一作用的详细机制尚不清楚。在此，我们研究了其对急性肺损伤（ALI）的保护作用，并进一步探讨了该作用的药理机制。我们发现，用其预处理可抑制ALI小鼠血清中促炎细胞因子的释放。肺组织的组织学分析表明，其可抑制脂多糖（LPS）诱导的肺损伤，改善肺形态，并减少肺中核因子-κB（NF-κB）的激活。此外，还研究了其抗炎作用。我们观察到，其可抑制用LPS刺激的RAW264.7细胞中白细胞介素-1（IL-1）、IL-6、单核细胞趋化蛋白-1（MCP-1）、环氧化酶-2（COX-2）和肿瘤坏死因子-α（TNF-α）的mRNA表达。此外，用其预处理可降低由LPS激活的p65和IκB-α的磷酸化水平。总之，我们的数据首次表明，其对ALI的抗炎作用是通过下调NF-κB信号通路实现的，从而减少炎症介质的产生。
