法半夏通过巨噬细胞和成纤维细胞的Crosstalk减轻COPD损伤机制研究OA
Mechanism study of Processed Pinellia ternata alleviating COPD in-jury through macrophages and fibroblasts Crosstalk
目的:探讨法半夏治疗慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)的作用机制.方法:将 40只雄性 C57BL/6J 小鼠随机分为对照组(n=8)、模型组(n=12)、法半夏组(1.5 g/kg,n=12)和氨茶碱组(1 mg/kg,n=8).采用烟熏联合脂多糖滴鼻法建立 COPD小鼠模型.HE 染色观察小鼠肺组织病理损伤,MASSON、MMP2和 MMP9的免疫组化染色检测肺组织纤维化,α-SMA 免疫组化染色检测肺组织成纤维细胞的转化,CD206和 F4/80免疫组化染色检测肺组织 M2巨噬细胞极化,qPCR 检测 TGF-β1和 Arg-1基 因 表 达,Western blot 检测肺组织中 Stat1、p-Stat1蛋白表达.此外,通过 Tran-swell 小室对巨噬细胞和成纤维细胞进行共培养,分为空白组、对照组、模型组、法半夏低、中、高剂量组(10、20、40 μg/mL),α-SMA 免疫荧光检测成纤维细胞的转化.结果:法半夏能明显减轻COPD 损伤(P<0.01),抑制肺组织增生和纤维化(P<0.001),降低 TGF-β1和 Arg-1基因相对表达量(P<0.05),抑制成纤维细胞的转化(P<0.05),减少 M2型巨噬细胞极化(P<0.05),增加 p-Stat1/Stat1比率(P<0.05).结论:法半夏通过阻断巨噬细胞和成纤维细胞的 Crosstalk 改善 COPD 的纤维化进程,可能与法半夏激活Stat1通路抑制 M2型巨噬细胞极化有关.
AIM:To explore the mechanism of Processed Pinellia ternata in treating chronic ob-structive pulmonary disease(COPD).METHODS:Forty male C57BL/6J mice were randomly divided into control group(n=8),model group(n=12),Pro-cessed Pinellia ternata group(1.5 g/kg,n=12),and aminophylline group(1 mg/kg,n=8).COPD model was established using smoke inhalation combined with lipopolysaccharide nasal drops.HE staining was employed to observe pathological damage in lung tissue.Lung tissue fibrosis was detected by Masson,MMP2,and MMP9 staining.Fibroblast transformation was tested α-SMA staining.CD206 and F4/80 staining were used to evaluated M2 macrophages polarization.The expression of TGF-β1 and Arg-1 genes were checked though qPCR,the level of Stat1 and p-Stat1 proteins were measured by Western blotting.In addition,macrophages and fibroblasts were co-cultured by transwell chambers,the(cells)were divided into blank control group,normal control group,model group,and low-,medi-um-,high-dose Pinellia ternata group groups(10,20,40 μg/mL,respectively),the fibroblasts transfor-mation was detected by α-SMA staining.RESULTS:Processed Pinellia ternata can significantly alleviate COPD injury(P<0.01),inhibit lung tissue prolifera-tion and fibrosis(P<0.001),reduce the relative ex-pression levels of TGF-β1 and Arg-1 genes(P<0.05),inhibit fibroblast transformation(P<0.05),reduce M2 macrophage polarization(P<0.05)and increase the p-Stat1/Stat1 ratio(P<0.05).CONCLUSION:Pro-cessed Pinellia ternata improves the fibrosis pro-cess in COPD by macrophages and fibroblasts crosstalk blocking,which may be related to sup-pressed M2 macrophage polarization and activated the Stat1 pathway.
魏宗烽;谭金龙;孙梦涵;朱乃亮;翟莹莹;陈琼;毕晶晶;梁利香;宋敏
信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南信阳农林学院药学院,信阳 464000,河南
医药卫生
法半夏慢性阻塞性肺疾病纤维化Crosstalk
Processed Pinellia ternatachronic obstructive pulmonary disease(COPD)fibrosisCrosstalk
《中国临床药理学与治疗学》 2026 (5)
585-595,11
国家自然科学基金青年项目(21702051)河南省自然科学基金面上项目(232300420065)河南省重点研发与推广专项(232102310364252102311246)河南省重大专项(241111311400)河南省高校重点科研项目(24B3600014)信阳农林学院青年基金项目(QN2023025QN2023028)
评论