The anti-inflammatory effects of baicalin through suppression of NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes
The anti-inflammatory effects of baicalin through suppression of NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes
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DOI：
10.1177/1753425916631032
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发表时间：
2016-04-01
期刊：
影响因子：
3.2
通讯作者：
Hou, Yongqing
中科院分区：
文献类型：
--
作者：
Ye, Chun;Li, Sali;Hou, Yongqing
本研究通过仔猪单核吞噬细胞（对照、LPS刺激、LPS刺激+12.5μg/ml黄芩苷、LPS刺激+25μg/ml黄芩苷、LPS刺激+50μg/ml黄芩苷、LPS）探讨黄芩苷对LPS诱导的NLRP3炎症通路的抗炎作用及机制。 刺激+100μg/ml黄芩苷）。体外LPS攻击后，活性氧（ROS）水平、IL-1、IL-18和TNF-的分泌水平、IL-1、IL-18、TNF-和NLRP3的mRNA表达水平以及cleaved caspase-1 p20的蛋白水平显着增加。然而，LPS 刺激并不影响凋亡相关斑点样蛋白和 caspase-1 mRNA 水平，它们也是 NLRP3 炎症小体的组成部分。 50μg/ml和100μg/ml黄芩苷可抑制ROS、TNF-、IL-1和IL-18的产生，下调IL-1、IL-18、TNF-和NLRP3的mRNA表达以及cleaved caspase-1 p20的表达。这些结果表明黄芩苷的抗炎作用是通过调节ROS的释放和NLRP3的mRNA表达来实现的。黄芩苷的抗炎活性可能与LPS刺激下NLRP3炎症小体通路的抑制有关。
In this study, the anti-inflammatory effects and mechanisms of baicalin on LPS-induced NLRP3 inflammatory pathway were investigated in piglet mononuclear phagocytes (control, LPS stimulation, LPS stimulation+12.5 mu g/ml baicalin, LPS stimulation+25 mu g/ml baicalin, LPS stimulation+50 mu g/ml baicalin and LPS stimulation+100 mu g/ml baicalin). The levels of reactive oxygen species (ROS), the secretion levels of IL-1, IL-18 and TNF-, mRNA expression levels of IL-1, IL-18, TNF- and NLRP3, as well as the protein levels of cleaved caspase-1 p20 were significantly increased after LPS-challenge invitro. However, LPS stimulation did not influence apoptosis-associated speck-like protein and caspase-1 mRNA levels, which are also components of the NLRP3 inflammasome. Baicalin at 50 mu g/ml and 100 mu g/ml could inhibit the production of ROS, TNF-, IL-1 and IL-18, and down-regulate mRNA expression of IL-1, IL-18, TNF- and NLRP3, as well as expression of cleaved caspase-1 p20. These results showed that the anti-inflammatory effects of baicalin occurred via the regulation of the release of ROS and mRNA expression of NLRP3. The anti-inflammatory activity of baicalin could be related to the suppression of NLRP3 inflammasome pathway under LPS stimulation.