Article(id=1292130349308473468, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.05.011, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1750521600000, receivedDateStr=2025-06-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997481895, onlineDateStr=2026-08-06, pubDate=1773676800000, pubDateStr=2026-03-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997481895, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997481895, creator=13701087609, updateTime=1785997481895, updator=13701087609, issue=Issue{id=1292130254689165893, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='5', pageStart='601', pageEnd='750', issueExtLink='null', onlineDate='null', pubDate='1773676800000', pubDateStr='2026-03-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997459337, creator='13701087609', updateTime=1786014469153, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201599108141219, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201599108141220, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=657, endPage=663, ext={EN=ArticleExt(id=1292130349501411453, articleId=1292130349308473468, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the effects of celastrol regulating the Notch pathway on the airway of lung fibroblasts in rats with chronic obstructive pulmonary disease, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of celastrol (Cel) on airway remodeling factors, collagen synthesis and degradation in lung fibroblasts of chronic obstructive pulmonary disease (COPD) rats by regulating the neurogenic locus notch homolog protein (Notch) pathway.
Methods A total of 30 rats were randomly divided into 3 groups: animal control group (normal feeding), animal model group (COPD rat model established by smoke exposure combined with lipopolysaccharide tracheal instillation) and animal experimental group (intraperitoneal injection of 0.01 mg·kg-1 Cel after successful modeling). The bronchial fibroblasts (BF) cells were isolated from rats in the animal model group and randomly divided into cell control group (no treatment), cell experimental group (2 μmol·L-1 Cel) and inhibitor group [1 mmol·L-1 valproic acid (VPA)]. Pulmonary function was assessed in rats using invasive pulmonary function testing methods; Western blot was used to detect the expression of Notch signaling pathway-related proteins in each group of cells; real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect mRNA expression of airway remodeling-related factors; enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of matrixmetalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) in each group of cells.
Results The forced vital capacity (FVC) of rats in animal control group, animal model group and animal experimental group were (6.74±0.87), (3.28±0.51) and (4.94±0.83) mL, respectively; the forced expiratory volume in 0.1 second (FEV0.1) were (3.94±0.45), (1.05±0.16) and (2.41±0.37) mL, respectively; the peak expiratory flow (PEF) were (28.09±4.60), (16.63±3.21) and (21.55±4.02) L·min-1, respectively. Significant differences were observed in the above indicators between animal control group and animal model group, and between animal model group and animal experimental group (P<0.01, P<0.001). The relative expression levels of (Notch1) protein in cell control group, cell experimental group and inhibitor group were 1.00±0.19, 0.12±0.02 and 0.38±0.06, respectively; the relative expression levels of Notch1 receptor intracellular binding domain (NICD1) protein were 1.00±0.17, 0.72±0.12 and 0.85±0.13, respectively; the relative expression levels of serrated typical Notch ligand 1 (Jagged1) protein were 1.00±0.15, 0.71±0.11 and 0.84±0.12, respectively; the relative expression levels of hair and enhancer of split 1 (Hes1) protein were 1.00±0.11, 0.69±0.08 and 0.81±0.09, respectively; the relative expression levels of MMP-9 mRNA were 1.00±0.16, 0.59±0.08 and 0.73±0.11, respectively; the relative expression levels of type Ⅰ collagen(ColⅠ) mRNA were 1.00±0.14, 0.67±0.09 and 0.86±0.14, respectively; the relative expression levels of α-smoth muscle actin (α-SMA) mRNA were 1.00±0.16, 0.41±0.07 and 0.78±0.13, respectively; the relative expression levels of transforming growth factor-β (TGF-β) mRNA were 1.00±0.18, 0.53±0.09 and 0.75±0.14, respectively; the contents of MMP-1 were (1.19±0.17), (0.80±0.15) and (1.06±0.15) ng·mL-1, respectively; the contents of tissue inhibitor of protease-1 (TIMP-1) were (219.78±30.24), (131.94±18.15) and (167.51±21.01) ng·mL-1, respectively. There were all statistically significant differences in the above indicators between cell control group and cell experimental group, as well as between cell experimental group and inhibitor group (P<0.05, P<0.01, P<0.001).
Conclusion Celastrol can effectively improve lung function and pulmonary pathological damage in COPD rats, reduce the levels of inflammatory cells and inflammatory factors, and improve the imbalance of airway remodeling-related factors and collagen synthesis/degradation in BF cells, which may be related to its inhibition of Notch signaling activation.
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目的 研究雷公藤红素（Cel）调控神经源性基因Notch同源蛋白（Notch）途径对慢阻肺（COPD）大鼠肺成纤维细胞气道重塑因子、胶原合成和降解的影响。
方法 30只大鼠随机分成动物对照组（正常饲养）、动物模型组（用烟熏结合脂多糖气管滴入法建立COPD大鼠模型）和动物试验组（造模成功后腹腔注射0.01 mg·kg-1 Cel）。取动物模型组大鼠，分离支气管成纤维（BF）细胞，随机分为细胞对照组（不做任何处理）、细胞实验组（2 μmol·L-1 Cel）和抑制剂组[1 mmol·L-1丙戊酸（VPA）]。用有创式肺功能检测法检测大鼠的肺功能；用蛋白质印迹法检测各组细胞内Notch信号通路相关蛋白的表达；用实时荧光定量聚合酶链反应（qRT-PCR）法检测各组细胞气道重塑相关因子和胶原合成相关指标mRNA表达；用酶联免疫吸附试验（ELISA）法检测各组细胞中基质金属蛋白酶-1（MMP-1）和蛋白酶组织抑制因子-1（TIMP-1）的含量。
结果 动物对照组、动物模型组和动物试验组大鼠的用力肺活量（FVC）分别为（6.74±0.87）、（3.28±0.51）和（4.94±0.83）mL，0.1 s用力呼气容积（FEV0.1）分别为（3.94±0.45）、（1.05±0.16）和（2.41±0.37）mL，呼气峰值流速（PEF）分别为（28.09±4.60）、（16.63±3.21）和（21.55±4.02）L·min-1，动物对照组与动物模型组相比、动物模型组与动物试验组相比，上述指标在统计学上差异均有统计学意义（P<0.01，P<0.001）。细胞对照组、细胞实验组和抑制剂组的Notch1蛋白相对表达水平分别为1.00±0.19、0.12±0.02和0.38±0.06，Notch1受体胞内结合域（NICD1）蛋白相对表达水平分别为1.00±0.17、0.72±0.12和0.85±0.13，锯齿状典型Notch配体1（Jagged1）蛋白相对表达水平分别为1.00±0.15、0.71±0.11和0.84±0.12，发状分裂相关增强子1（Hes1）蛋白相对表达水平分别为1.00±0.11、0.69±0.08和0.81±0.09；MMP-9 mRNA相对表达水平分别为1.00±0.16、0.59±0.08和0.73±0.11，Ⅰ型胶原（ColⅠ）mRNA相对表达水平分别为1.00±0.14、0.67±0.09和0.86±0.14，α-平滑肌肌动蛋白（α-SMA）mRNA相对表达水平分别为1.00±0.16、0.41±0.07和0.78±0.13，转化生长因子-β（TGF-β）mRNA相对表达水平分别为1.00±0.18、0.53±0.09和0.75±0.14，MMP-1含量分别为（1.19±0.17）、（0.80±0.15）和（1.06±0.15）ng·mL-1，TIMP-1分别为（219.78±30.24）、（131.94±18.15）和（167.51±21.01）ng·mL-1，细胞对照组与细胞实验组相比、细胞实验组与抑制剂组相比，上述指标在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。
结论 Cel能够有效改善COPD大鼠的肺功能和肺部病理损伤、降低炎症细胞及炎症因子的水平、改善BF细胞气道重塑相关因子水平及胶原合成和降解失衡，可能与其抑制Notch信号的激活有关。
, authors=李莎莎, 邱日皇, authorsList=李莎莎, 邱日皇, authorCompany=null, correspAuthors=邱日皇, authorNote=
李莎莎（1990-），女，主治医师，主要从事慢阻肺方面的研究
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