Song Dan, Wei Wenfeng, Zhang Jie, Zhang Lu, Wang Weiming, Huo Jinhai
Traditional Chinese Medicine, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang, China.
Nursing, Heilongjiang Nursing College, Harbin, China.
Immunol Invest. 2025 May;54(4):560-572. doi: 10.1080/08820139.2025.2450244. Epub 2025 Jan 9.
This study investigated the mechanism of baicalin (BIA) attenuating the inflammatory response and lung injury in mycoplasma pneumoniae pneumonia (MPP) mice.
MPP mouse models were established and then treated with BIA, azithromycin, or NLRP3 inflammasome activator. Lung wet-to-dry weight (W/D) ratio were weighed. Serum levels of MP-IgM, C-reactive protein (CRP) and bronchoalveolar lavage fluid (BALF) protein were detected by kits, NLRP3/Caspase-1 pathway-related protein levels by Western blot, and IL-1β, IL-18, IL-6 and TNF-α levels by ELISA. HE staining was performed to detect lung injury.
MPP mice showed elevated mouse lung W/D ratio, upregulated serum MP-IgM and CRP levels and BALF protein, and enhanced IL-6 and TNF-α levels, which were reversed by BIA or azithromycin treatment, suggesting that BIA attenuated pulmonary inflammatory response in MPP mice. The lung tissue of MPP mice showed upregulated NLRP3, cleaved Caspase-1,Caspase-1, GSDMD-N and GSDMD levels and raised IL-1β and IL-18 levels, and changes were annulled by BIA or azithromycin treatment, suggesting that BIA inhibited the NLRP3/Caspase-1 pathway activation. NLRP3/Caspase-1 pathway activation partially abrogated the alleviative effect of BIA on the pulmonary inflammatory response of MPP mice.
BIA mitigates inflammatory response and lung injury in MPP mice by inhibiting NLRP3/Caspase-1 pathway activation.
本研究探讨黄芩苷（BIA）减轻肺炎支原体肺炎（MPP）小鼠炎症反应和肺损伤的机制。
建立MPP小鼠模型，然后用BIA、阿奇霉素或NLRP3炎性小体激活剂进行治疗。称取肺组织湿重与干重之比（W/D）。采用试剂盒检测血清中MP-IgM、C反应蛋白（CRP）水平以及支气管肺泡灌洗液（BALF）蛋白含量，采用蛋白质免疫印迹法检测NLRP3/Caspase-1通路相关蛋白水平，采用酶联免疫吸附测定法检测白细胞介素-1β（IL-1β）、白细胞介素-18（IL-18）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平。进行苏木精-伊红（HE）染色以检测肺损伤情况。
MPP小鼠肺组织W/D比值升高，血清MP-IgM和CRP水平以及BALF蛋白含量上调，IL-6和TNF-α水平升高，而BIA或阿奇霉素治疗可使其逆转，提示BIA减轻了MPP小鼠的肺部炎症反应。MPP小鼠肺组织中NLRP3、裂解的Caspase-1、Caspase-1、Gasdermin-D N端（GSDMD-N）和GSDMD水平上调，IL-1β和IL-18水平升高，BIA或阿奇霉素治疗可消除这些变化，提示BIA抑制了NLRP3/Caspase-1通路的激活。NLRP3/Caspase-1通路激活部分抵消了BIA对MPP小鼠肺部炎症反应的缓解作用。
BIA通过抑制NLRP3/Caspase-1通路激活减轻MPP小鼠的炎症反应和肺损伤。
