Article(id=1291404896528495326, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.08.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1729094400000, receivedDateStr=2024-10-17, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824520475, onlineDateStr=2026-08-04, pubDate=1745769600000, pubDateStr=2025-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824520475, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824520475, creator=13701087609, updateTime=1785824520475, updator=13701087609, issue=Issue{id=1291404807152067353, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1745769600000', pubDateStr='2025-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824499166, creator='13701087609', updateTime=1785824499166, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1102, endPage=1107, ext={EN=ArticleExt(id=1291404896859845343, articleId=1291404896528495326, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of carbocisteine on airway inflammation and airway remodeling in mice with
Mycoplasma pneumoniae pneumonia based on p38MAPK/AP-1 signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To study the effects of carbocisteine on airway inflammation and airway remodeling in mice with Mycoplasma pneumoniae pneumonia and its mechanism.
Methods Mice were randomly divided into control group, model group, experimental group, negative transfection group and positive transfection group, with 12 mice in each group. The control group were inoculated with 0.9% NaCl by nasal drip, the other groups were inoculated with Mycoplasma pneumoniae suspension to establish Mycoplasma pneumoniae pneumonia model. After successful modeling, the experimental group was given 10 mg·kg-1 carbocisteine by intragastric administration; the negative transfection group was given 10 mg·kg-1 carbocisteine by gavage + 1.0×109 PFU of adenovirus containing tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) blank control plasmid in the tail vein, the positive transfection group was given 10 mg·kg-1 carbocisteine by intragastrial + 1.0×109 PFU containing sh-TIPE2 plasmid was injected into the tail vein, the control and model groups were given 0.9% NaCl by intragastric administration. Five groups were treated for 2 weeks with once a day. The levels of inflammatory factors in lung tissue were detected by enzyme-linked immunosorbent assay. Airway remodeling index and p38 mitogen activated protein kinase (p38MAPK) /activated protein-1 (AP-1) signaling pathway related protein expression were detected by Western blot.
Results The levels of tumor necrosis factor-α in control, model, experimental, negative transfection and positive transfection groups were (9.18±1.92), (134.32±24.56), (42.20±8.61), (39.95±7.77) and (74.03±13.59) pg·mL-1; the levels of interleukin-6 were (5.80±1.21), (65.12±11.81), (22.94±4.47), (26.11±5.08) and (42.67±7.97) pg·mL-1; the relative protein expression levels of matrix metallopeptidase 9 were 1.00±0.16, 3.64±0.62, 1.45±0.22, 1.39±0.20 and 2.16±0.38; the relative protein expression levels of tissue inhibitor of metalloproteinases 1 were 1.00±0.14, 0.52±0.11, 0.89±0.16, 0.84±0.15 and 0.65±0.13; the phospho-p38MAPK/p38MAPK ratios were 1.00±0.16, 2.74±0.48, 1.57±0.29, 1.54±0.27 and 2.31±0.36; the relative protein expression levels of cellular proto-oncogene Jun were 1.00±0.14, 2.25±0.38, 1.34±0.21, 1.37±0.22 and 1.98±0.32; the relative protein expression levels of cellular proto-oncogene Fos were 1.00±0.18, 3.07±0.56, 1.86±0.32, 1.91±0.35 and 2.51±0.44, respectively. The above indexes in the model group were compared with the experimental and control groups, the above indexes in the positive transfection group were compared with the negative transfection group, and the differences were statistically significant (all P<0.05).
Conclusion Carbocisteine inhibits airway inflammation and airway remodeling in mice with Mycoplasma pneumoniae pneumonia by inhibiting the p38MAPK/AP-1 signaling pathway.
, authors=Ning-xiang WANG, Hui LI, Xin TAN, authorsList=Ning-xiang WANG, Hui LI, Xin TAN, authorCompany=null, correspAuthors=Xin TAN, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291404897342190304, articleId=1291404896528495326, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于p38MAPK/AP-1信号通路探索羧甲司坦对肺炎支原体肺炎小鼠气道炎症和气道重塑的影响, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 研究羧甲司坦对肺炎支原体肺炎小鼠气道炎症和气道重塑的影响，及其作用机制。
方法 将小鼠随机分为正常组、模型组、实验组、阴性转染组和阳性转染组，每组12只。正常组滴鼻接种等量的0.9% NaCl，其余组小鼠均滴鼻接种肺炎支原体混悬液建立肺炎支原体肺炎模型。在造模成功后，实验组灌胃给予10 mg·kg-1的羧甲司坦；阴性转染组灌胃给予10 mg·kg-1的羧甲司坦+尾静脉注射含有肿瘤坏死因子α诱导蛋白8样分子2（TIPE2）空白对照序列质粒的腺病毒1.0×109 PFU；阳性转染组灌胃给予10 mg·kg-1的羧甲司坦+尾静脉注射含有sh-TIPE2序列质粒的腺病毒1.0×109 PFU；正常组和模型组均灌胃给予等量的0.9% NaCl。5组小鼠每天给药1次，连续2周。用酶联免疫吸附试验法检测各组小鼠肺组织炎症因子水平，用蛋白质印迹法检测气道重塑指标、p38丝裂原活化蛋白激酶（p38MAPK）/激活蛋白1（AP-1）信号通路相关蛋白的表达情况。
结果 正常组、模型组、实验组、阴性转染组和阳性转染组的肿瘤坏死因子-α水平分别为（9.18±1.92）、（134.32±24.56）、（42.20±8.61）、（39.95±7.77）和（74.03±13.59）pg·mL-1，白细胞介素-6水平分别为（5.80±1.21）、（65.12±11.81）、（22.94±4.47）、（26.11±5.08）和（42.67±7.97）pg·mL-1，基质金属蛋白酶9蛋白相对表达水平分别为1.00±0.16、3.64±0.62、1.45±0.22、1.39±0.20和2.16±0.38，金属蛋白酶组织抑制因子-1蛋白相对表达水平分别为1.00±0.14、0.52±0.11、0.89±0.16、0.84±0.15和0.65±0.13，磷酸化p38MAPK/p38MAPK比值分别为1.00±0.16、2.74±0.48、1.57±0.29、1.54±0.27和2.31±0.36，细胞核因子Jun蛋白相对表达水平分别为1.00±0.14、2.25±0.38、1.34±0.21、1.37±0.22和1.98±0.32，细胞核因子Fos蛋白相对表达水平分别为1.00±0.18、3.07±0.56、1.86±0.32、1.91±0.35和2.51±0.44。模型组的上述指标与实验组和正常组比较，阳性转染组的上述指标与阴性转染组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 羧甲司坦通过抑制p38MAPK/AP-1信号通路来抑制肺炎支原体肺炎小鼠的气道炎症和气道重塑。
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王宁湘（1988），女，主治医师，主要从事小儿重症方面的临床诊疗工作
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