摘要
目的:探讨清热化湿抗毒方(QRHS)对湿热壅肺型肺损伤小鼠的治疗作用及其机制。方法:60只C57BL/6雄性小鼠随机分为正常组,模型组,QRHS低、中、高剂量组及醋酸泼尼松(PAT)组。除正常组外,其余组通过湿热刺激联合脂多糖诱导肺损伤并使用相应药物治疗。HE染色观察肺组织病理变化;检测白细胞计数、中性粒细胞计数和血小板计数;利用流式细胞术评估M1/M2型巨噬细胞水平;ELISA检测肺组织中白细胞介素(IL)-2、IL-6、干扰素-γ(IFN-γ)、转化生长因子-β(TGF-β)、免疫球蛋白(Ig)G、IgA和IgM水平;Western Blot检测肺组织中活化B细胞核因子κ轻链增强子(NF-κB)p65、p-NF-κB p65、核因子κB受体激活因子(RANK)、核因子κB受体激活因子配体(RANKL)蛋白水平。结果:与模型组比较,QRHS各组肺泡壁厚度、坏死面积及炎症浸润均减少;肺组织中IL-2、IL-6、IFN-γ、IgG、IgA、IgM水平显著降低(除QRHS-L组的IL-2外)(P<0.05,P<0.01),TGF-β水平显著升高(P<0.01);单核及巨噬细胞数量显著下降(P<0.01,P<0.05),M1型巨噬细胞显著减少(P<0.01,P<0.05),M2型巨噬细胞显著增加(P<0.05,P<0.01);QRHS-H组NF-κB p65、p-NF-κB p65、RANK、RANKL蛋白表达显著降低(P<0.01,P<0.05)。结论:QRHS通过下调NF-κB/RANK/RANKL信号通路抑制M1型巨噬细胞并促进M2型巨噬细胞极化,有效治疗湿热壅肺型肺损伤。
Objective:To investigate the therapeutic effects of Qingre Huashi Kangdu Formula(QRHS)on lung injury in mice with dampness-heat obstructing the lung syndrome and explore its underlying mechanisms.Methods:Sixty male C57BL/6 mice were randomly divided into six groups:control group,model group,QRHS low-dose group,QRHS medium-dose group,QRHS highdose group,and prednisone acetate(PAT)group.Except for the control group,all other groups were subjected to lung injury induced by dampness-heat stimulation,combined with lipopolysaccharide and treated with corresponding drugs.Pathological changes in lung tissue were observed using HE staining.Levels of white blood cells,neutrophils,and platelets were measured.Flow cytometry was used to assess M1/M2 macrophage polarization.ELISA was used to measure the levels of interleukin(IL)-2,IL-6,interferon-γ(IFN-γ),transforming growth factor-β(TGF-β),immunoglobulin(Ig)G,IgA,and IgM in lung tissue.Western Blot was used to measure the protein levels of NF-κB p65,p-NF-κB p65,RANK and RANKL in lung tissue.Results:Compared with the model group,the QRHS groups showed reduced alveolar wall thickness,decreased necrotic area,and alleviated inflammatory infiltration,levels of IL-2,IL-6,IFN-γ,IgG,IgA,and IgM in lung tissue were significantly decreased(expect for the level of IL-2 in QRHS low-dose group)(P<0.05,P<0.01),the level of TGF-βwas significantly increased(P<0.01),the total number of monocytes and macrophages significantly decreased(P<0.01,P<0.05),with a significantly reduction in M1 macrophages(P<0.01,P<0.05)and a significantly increase in M2 macrophages(P<0.05,P<0.01),protein expression of NF-κB p65,p-NF-κB p65,RANK,and RANKL in QRSH highdose group also significantly reduced(P<0.01,P<0.05).Conclusion:QRHS effectively treates mice with damp-heat-heat congested lung injury by down-regulating the NF-κB/RANK/RANKL signaling pathway,inhibiting M1-type macrophages and promoting M2-type macrophage polarization.
作者
郑林欣
周步高
李姗姗
王阳
李思莉
汪慧玉
林雨含
刘端勇
ZHENG Linxin;ZHOU Bugao;LI Shanshan;WANG Yang;LI Sili;WANG Huiyu;LIN Yuhan;LIU Duanyong(Graduate School,Jiangxi University of Chinese Medicine,Nanchang 330004,China;School of Traditional Chinese Medicine,Jiangxi University of Chinese Medicine,Nanchang 330004,China;Jiangxi Provincial Key Laboratory of Formula-Exemplification Research,Nanchang 330004,China;Laboratory Animal Science and Technology Center,Jiangxi University of Chinese Medicine,Nanchang 330004,China;School of Nursing,Jiangxi University of Chinese Medicine,Nanchang 330004,China)
出处
《中华中医药杂志》
北大核心
2025年第5期2151-2156,共6页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
江西省2022年度中央引导地方科技发展资金(第二批)(No.20222ZDH01096)
国家中医药管理局青年岐黄学者支持项目(No.国中医药人教函[2022]256号)
2020年度江西省工程研究中心项目(No.赣发改高技[2020]1048号)
南昌市科学技术局重点实验室项目(No.洪科字[2024]87号)
国家自然科学基金项目(No.82060798)。
