黄芩苷通过miR-181b/HMGB1/TRL4/NF-κB途径抑制LPS诱导的RAW264.7细胞炎症。
Baicalin inhibits LPS-induced inflammation in RAW264.7 cells through miR-181b/HMGB1/TRL4/NF-κB pathway.
作者信息
Yan Guoliang, Chen Liyun, Wang Haihui, Wu Sai, Li Shufang, Wang Xinlu
机构信息
ICU Department, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine Shanghai 200071, China.
Emergency Department, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 200021, China.
出版信息
Am J Transl Res. 2021 Sep 15;13(9):10127-10141. eCollection 2021.
PURPOSE
Inflammation out of control may induce many diseases. Baicalin has certain anti-inflammatory effects, but its mechanism of action is not clear. Therefore, this study was designed to explore a potential mechanism of anti-inflammation.
METHODS
In this study, RAW264.7 cells were induced by 1.0 g/mL lipopolysaccharide (LPS) and then exposed to baicalin at various concentrations (0.1-1.0 μmol/L). Then, we investigated the effect of baicalin in RAW264.7 inflammation models.
RESULTS
In this study, 0.1-1.0 μmol/L baicalin, especially baicalin at 1.0 μmol/L, effectively inhibited the expression of inflammatory factors (TNF-α, IL-1β, IL-6, Cox, and iNOS), decreased the activity of High Mobility Group Box 1 (HMGB1)/Toll-like Receptor 4 (TLR4)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, and stimulated miR-181b expression. HMGB1 was proved to be negatively regulated by miR-181b. Here, up-regulation of miR-181b or down-regulation of HMGB1 exerted similar effects as baicalin and down-regulated miR-181b reversed the anti-inflammatory effect of baicalin in RAW264.7 inflammation models.
CONCLUSION
Baicalin can inhibit LPS-induced inflammation in RAW264.7 cells via the miR-181b/HMGB1/TRL4/NF-κB pathway.
目的
炎症失控可能诱发多种疾病。黄芩苷具有一定的抗炎作用，但其作用机制尚不清楚。因此，本研究旨在探索一种潜在的抗炎机制。
方法
在本研究中，用1.0 g/mL脂多糖（LPS）诱导RAW264.7细胞，然后将其暴露于不同浓度（0.1 - 1.0 μmol/L）的黄芩苷中。然后，我们研究了黄芩苷在RAW264.7炎症模型中的作用。
结果
在本研究中，0.1 - 1.0 μmol/L的黄芩苷，尤其是1.0 μmol/L的黄芩苷，有效抑制了炎症因子（TNF-α、IL-1β、IL-6、Cox和iNOS）的表达，降低了高迁移率族蛋白B1（HMGB1）/Toll样受体4（TLR4）/活化B细胞核因子κB（NF-κB）通路的活性，并刺激了miR-181b的表达。HMGB1被证明受miR-181b负调控。在此，miR-181b的上调或HMGB1的下调产生了与黄芩苷相似的作用，而miR-181b的下调逆转了黄芩苷在RAW264.7炎症模型中的抗炎作用。
结论
黄芩苷可通过miR-181b/HMGB1/TRL4/NF-κB通路抑制LPS诱导的RAW264.7细胞炎症。
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