Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity
Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity
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黄芩苷在香烟烟雾诱导的体内和体外炎症模型中具有抗炎作用：HDAC2 活性的可能作用
DOI：
10.1016/j.intimp.2012.03.001
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发表时间：
2012-05-01
影响因子：
5.6
通讯作者：
Dong, Jingcheng
中科院分区：
文献类型：
--
作者：
Li, Lulu;Bao, Hong;Dong, Jingcheng
慢性阻塞性肺疾病（COPD）是一种以气道阻塞和进行性肺部炎症为特征的慢性炎症性疾病，对皮质类固醇治疗不敏感。在这项研究中，我们在体内和体外研究了黄芩苷（一种从黄芩根中分离出来的黄酮类化合物）减轻香烟烟雾（CS）引起的呼吸道炎症的机制。在体内，小鼠每天 1 小时、每周 6 天接触 15 支香烟的烟雾，持续 3 个月，并给予黄芩苷（25、50 和 100 mg/kg）或地塞米松（1 mg/kg）。在体外，A549细胞与黄芩苷（10、50和100μM）或地塞米松（10（-12）、10（-10）、10（-8）和10（-6）M）一起孵育，然后用香烟烟雾提取物（CSE，2.5和5％）或TNF-α（10ng/ml）或曲古抑菌素A处理（TSA，100 纳克/毫升）。我们发现黄芩苷通过减少炎症细胞和 TNF-α、IL-8 和 MMP-9 的产生，显着保护肺功能并减轻 CS 诱导的炎症反应。在用地塞米松治疗的组中未发现该结果。黄芩苷还显示出增强组蛋白脱乙酰酶 (HDAC)2 活性和蛋白质表达的功效，但它并不影响 HDAC2 mRNA。进一步研究发现黄芩苷可抑制HDAC2磷酸化，提示其可能通过翻译后水平的修饰直接影响蛋白质的结构和作用。这些结果表明，黄芩苷在小鼠和 A549 细胞中香烟烟雾诱导的炎症模型中具有抗炎作用，这可能是通过调节 HDAC2 来实现的。 (C) 2012 Elsevier B.V. 保留所有权利。
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by airway obstruction and progressive lung inflammation, which is insensitive to corticosteroids therapies. In this study, we investigated the mechanism underlying the attenuation of cigarette smoke (CS)-induced respiratory inflammation by baicalin, a flavonoid compound isolated from the root of Scutellaria baicalensis Georgi, in vivo and in vitro. In vivo, mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with baicalin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). In vitro, A549 cells were incubated with baicalin (10, 50 and 100 mu M) or dexamethasone (10(-12), 10(-10), 10(-8) and 10(-6) M) followed by treatments with cigarette smoke extract (CSE, 2.5 and 5%), or TNF-alpha (10 ng/ml), or trichostatin A (TSA, 100 ng/ml). We found that baicalin significantly protected pulmonary function and attenuated CS-induced inflammatory response by decreasing inflammatory cells and production of TNF-alpha, IL-8 and MMP-9. This result was not found in the group treated with dexamethasone. Baicalin also showed efficacy in enhancing histone deacetylase (HDAC)2 activity and protein expression, however, it did not affect HDAC2 mRNA. Further studies revealed that baicalin inhibited HDAC2 phosphorylation, suggesting that it may directly affect the protein structure and effect by modification at post-translational level. Together these results suggest that baicalin has anti-inflammatory effects in cigarette smoke induced inflammatory models in mice and A549 cells, possibly achieved by modulating HDAC2. (C) 2012 Elsevier B.V. All rights reserved.