首页|基于TLR2/NF-κB信号通路探讨茵陈清肺颗粒对肺炎支原体肺炎小鼠的调控作用及机制

基于TLR2/NF-κB信号通路探讨茵陈清肺颗粒对肺炎支原体肺炎小鼠的调控作用及机制

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目的:探究茵陈清肺颗粒治疗肺炎支原体肺炎(MPP)的作用机制和有效靶点.方法:选取SPF级BALB/c小鼠36只,普通饲料适应性喂养3 d后,随机选取6只作为空白组,剩余30只采用肺炎支原体(MP)菌液滴鼻联合高脂饮食和外环境法建立湿热闭肺证模型.成功建立模型后随机分为模型组、阿奇霉素组(给予阿奇霉素90.1 mg·kg-1·d-1)、茵陈清肺颗粒高(8.109 g·kg-1·d-1、)、中(5.406 g·kg-1·d-1)、低剂量组(2.703 g·kg-1·d-1),模型组及空白组灌服等体积0.9%生理盐水.给药3 d后,在末次给药4 h后取材,HE染色观察小鼠肺组织病理变化;RT-qPCR技术检测肺组织TLR2、MyD88、NF-κB p65 mRNA 表达水平;Western blot 技术检测肺组织 TLR2、MyD88、NF-κB p65 蛋白表达水平.结果:HE染色结果表明,空白组可见肺泡结构清晰,模型组出现肺实变,大量炎性细胞浸润,血管内大量出血,各给药组均能改善小鼠肺组织病变、细胞浸润及炎症程度.mRNA表达水平检测结果表明,与空白组比较,模型组TLR2、MyD88以及NF-κB p65的mRNA表达显著增高(P<0.01),与模型组比较,除茵陈清肺颗粒低剂量组NF-κB p65外,其余给药组的mRNA表达显著降低(P<0.05,P<0.01),茵陈清肺颗粒高剂量组TLR2 mRNA表达低于阿奇霉素组(P<0.05).蛋白表达水平检测结果表明,与空白组比较,模型组TLR2、MyD88以及NF-κB p65的蛋白表达水平明显升高(P<0.01),除茵陈清肺颗粒中剂量组MyD88、NF-κBp65蛋白表达外,其他给药组通路蛋白表达均显著低于模型组(P<0.05,P<0.01).结论:茵陈清肺颗粒能明显改善MP小鼠肺组织炎性症状,其机制可能与抑制 TLR2/NF-κB信号通路相关.
Regulatory Effects and Mechanism of Yinchen Qingfei Granules on Mycoplasma Pneumoniae Pneumonia in Mice Based on the TLR2/NF-κB Signaling Pathway
Objective:To investigate the mechanism and effective targets of Yinchen Qingfei Granules in treating Mycoplasma Pneumoniae Pneumonia(MPP).Methods:Thirty-six SPF-grade BALB/c mice were used.After 3 days of adaptive feeding with standard diet,6 mice were randomly selected as the blank group,and the remaining 30 mice were subjected to nasal instillation of Mycoplasma Pneumoniae(MP)bacterial solution combined with high-fat diet and environmental exposure to establish a model of damp-heat obstructing lung syndrome.After the model was successfully established,the mice were randomly divided into model group,azithromycin group(administered azithromycin 90.1 mg·kg-1·d-1),and low(8.109 g·kg-1·d-1),medium(5.406 g·kg-1·d-1),and high-dose(2.703 g·kg-1·d-1)Yinchen Qingfei Granules groups.The model and blank groups were given an equal volume of 0.9%saline.After 3 days of treatment,tissues were collected 4 hours after the last dose for analysis.HE staining was used to observe the pathological changes in the lung tissue of the mice;RT-qPCR was used to detect the mRNA expression of TLR2,MyD88,and NF-κBp65 in lung tissue;Western blot was used to detect the protein expression levels of TLR2,MyD88,and NF-κBp65 in lung tissue.Results:HE staining showed that the alveolar structure was clear in the blank group,while the model group exhibited lung consolidation,extensive inflammatory cell infiltration,and significant hemorrhage in the vessels.Lung tissue lesions,cellular infiltration,and inflammation were improved in all treatment groups.Compared to the blank group,the mRNA expression of TLR2,MyD88,and NF-κBp65 significantly increased in the model group(P<0.01).Compared to the model group,mRNA expression levels of TLR2 and NF-κBp65 were significantly decreased in all treatment groups except the low-dose group(P<0.05),with the high-dose Yinchen Qingfei Granules group having lower TLR2 mRNA expression than the azithromycin group(P<0.05).Compared to the blank group,the protein expression levels of TLR2,MyD88,and NF-κBp65 were significantly increased in the model group(P<0.05).Except for the medium-dose Yinchen Qingfei Granules group where MyD88 and NF-κBp65 protein levels were not significantly different,other treatment groups had significantly lower pathway protein expression than the model group(P<0.05).Conclusion:Yinchen Qingfei Granules can significantly improve inflammatory symptoms in MP-infected mouse lung tissue,and its mechanism may be related to the inhibition of the TLR2/NF-κB signaling pathway.

TLR2/NF-κBMycoplasma penumoniae PneumoniaDampness-dispelling and collaterals-unblockingYinchen Qingfei Granules

王睿昊、张葆青、贾广媛、周旭

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山东中医药大学第一临床医学院,山东济南 250011

山东省中医院,山东济南 250011

TLR2/NF-κB 肺炎支原体肺炎 祛湿通络 茵陈清肺颗粒

2025

中医药学报
中华中医药学会,黑龙江中医药大学

中医药学报

影响因子:1.169
ISSN:1002-2392
年,卷(期):2025.53(1)