Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.
Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.
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DOI：
10.1186/s10020-021-00309-z
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发表时间：
2021-05-30
期刊：
影响因子：
--
通讯作者：
Jiang J
中科院分区：
文献类型：
--
作者：
Hao D;Li Y;Shi J;Jiang J
慢性阻塞性肺疾病（COPD）的特征是气道阻塞和进行性肺部炎症。黄芩苷作为一种传统中药的主要成分，以前已被证明具有抗炎能力。因此，本研究旨在阐明黄芩苷治疗COPD的机制。采用黄芩苷处理香烟烟雾提取物暴露的MLE-12细胞，检测细胞存活率和凋亡率。采用酶联免疫法测定肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、IL-8的含量。通过香烟烟雾和脂多糖暴露、黄芩苷治疗建立COPD小鼠模型。检测肺功能、炎性细胞浸润，ELISA法检测支气管肺泡灌洗液（BALF）中Muc 5AC、TNF-α、IL-6、IL-8的含量。通过体内和体外功能丧失和获得实验，评估黄芩苷治疗后HSP 72和JNK对COPD的影响。黄芩苷可改善小鼠肺功能，表现为炎性细胞浸润减少，BALF中Muc 5AC、TNF-α、IL-6和IL-8水平降低。黄芩苷可提高MLE-12细胞活力，抑制细胞凋亡，降低TNF-α、IL-6和IL-8水平。黄芩苷治疗增加HSP 72的表达，而其消耗逆转黄芩苷对COPD的影响。HSP 72抑制JNK的激活，而JNK的激活则抑制黄芩苷对COPD的作用。黄芩苷上调HSP 72的表达，抑制JNK信号通路的激活，最终导致COPD的加重。在线版本包含补充材料，可通过10.1186/s10020-021-00309-z获得。
Chronic obstructive pulmonary disease (COPD) is characterized by airway obstruction and progressive lung inflammation. As the primary ingredient of a traditional Chinese medical herb, Baicalin has been previously shown to possess anti-inflammatory abilities. Thus, the current study aimed to elucidate the mechanism by which baicalin alleviates COPD. Baicalin was adopted to treat cigarette smoke in extract-exposed MLE-12 cells after which cell viability and apoptosis were determined. The production of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-8 were determined by enzyme-linked immunoassay. A COPD mouse model was constructed via exposure to cigarette smoke and lipopolysaccharide, baicalin treatment. Lung function and inflammatory cell infiltration were determined and the production of Muc5AC, TNF-α, IL-6, IL-8 in the bronchoalveolar lavage fluid (BALF) was assayed by ELISA. The effect of HSP72 and JNK on COPD following treatment with baicalin was assessed both in vivo and in vitro by conducting loss- and gain- function experiments. Baicalin improved lung function evidenced by reduction in inflammatory cell infiltration and Muc5AC, TNF-α, IL-6 and IL-8 levels observed in BALF in mice. Baicalin was further observed to elevate cell viability while inhibited apoptosis and TNF-α, IL-6 and IL-8 levels in MLE-12 cells. Baicalin treatment increased HSP72 expression, while its depletion reversed the effect of baicalin on COPD. HSP72 inhibited the activation of JNK, while JNK activation was found to inhibit the effect of baicalin on COPD. Baicalin upregulated the expression of HSP72, resulting in the inhibition of JNK signaling activation, which ultimately alleviates COPD. The online version contains supplementary material available at 10.1186/s10020-021-00309-z.
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