Article(id=1291404936227573833, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.08.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1728489600000, receivedDateStr=2024-10-10, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824529939, onlineDateStr=2026-08-04, pubDate=1745769600000, pubDateStr=2025-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824529939, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824529939, creator=13701087609, updateTime=1785824529939, 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=1091, endPage=1095, ext={EN=ArticleExt(id=1291404936424706122, articleId=1291404936227573833, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of hydroxysafflor yellow A on neutrophil migration in acute exacerbation of chronic obstructive pulmonary disease mice, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the therapeutic effect of hydroxysafflor yellow A (HSYA) on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) mice and its mechanism of action.
Methods Mice were randomly divided into control group, model group and experimental -L, -M, -H groups, with 20 mice per group. The control group was raised normally, and the other groups were exposed to cigarette smoke (CS) and non-typeable Haemophilus influenzae (NTHi) infection to establish an AECOPD mouse model. Starting from the 12th week of CS exposure, experimental -L, -M, -H groups were administered 25, 50 and 100 mg·kg-1·d-1 HSYA by gavage, and control and model groups were given 0.9% NaCl by gavage. Five groups were administered once a day for 2 weeks. The functional residual capacity (FRC) of the mice was measured using the Buxco lung function test system. The percentage of neutrophils in bronchoalveolar lavage fluid (BALF) was measured using flow cytometry. The expression levels of phosphatidylinositol-3-kinase (PI3K) and protein kinase B (Akt) in lung tissues were detected by Western blot.
Results The FRC of experimental -M, -H groups, model group and control group were (0.31±0.01), (0.27±0.01), (0.37±0.02) and (0.25±0.01) L; the neutrophil percentages were (37.96±2.88)%, (28.41±1.64)%, (60.27±2.12)% and (11.33±0.31)%; the phosphorylated PI3K/PI3K ratios were 1.59±0.08, 1.30±0.06, 2.28±0.08 and 1.00±0.06; the phosphorylated Akt/Akt ratios were 1.33±0.11, 1.15±0.03, 1.76±0.11 and 1.00±0.06, respectively. Compared with model group, the differences of above indexes in experimental -M, -H groups were statistically significant (all P<0.05).
Conclusion HSYA may reduce neutrophil activity by inhibiting the PI3K/Akt pathway, thereby inhibiting inflammatory responses and alleviating lung injury.
, authors=Zhong-fang WANG
1, Zi-min JI
2a, Zhi-qiang LIN
2b, Yong-bing LI
2a, Jian-hua LÜ
2a, authorsList=Zhong-fang WANG, Zi-min JI, Zhi-qiang LIN, Yong-bing LI, Jian-hua LÜ, authorCompany=null, correspAuthors=Zi-min JI, 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=1291404936907051083, articleId=1291404936227573833, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=羟基红花黄色素A对慢性阻塞性肺疾病急性加重期小鼠中性粒细胞迁移的影响, 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 探索羟基红花黄色素A（HSYA）对慢性阻塞性肺疾病急性加重期（AECOPD）小鼠的治疗作用，及其作用机制。
方法 将小鼠随机分为对照组、模型组和低、中、高剂量实验组，每组20只。对照组正常饲养，其他组通过基于香烟烟雾（CS）和不可分型的流感嗜血杆菌感染来建立AECOPD小鼠模型。从CS暴露第12周开始，低、中、高剂量实验组分别灌胃给予25、50、100 mg·kg-1·d-1 HSYA，对照组和模型组均灌胃给予等量0.9% NaCl。5组小鼠每天给药1次，连续给药2周。用Buxco肺功能测试系统检测小鼠功能残气量（FRC），用流式细胞仪检测支气管肺泡灌洗液（BALF）中的中性粒细胞百分比，用蛋白质印迹法检测肺组织中磷脂酰肌醇-3-激酶（PI3K）和蛋白激酶B（Akt）的表达水平。
结果 中、高剂量实验组和模型组、对照组的FRC分别为（0.31±0.01）、（0.27±0.01）、（0.37±0.02）和（0.25±0.01）L，中性粒细胞百分比分别为（37.96±2.88）%、（28.41±1.64）%、（60.27±2.12）%和（11.33±0.31）%，磷酸化PI3K/PI3K比值分别为1.59±0.08、1.30±0.06、2.28±0.08和1.00±0.06，磷酸化Akt/Akt比值分别为1.33±0.11、1.15±0.03、1.76±0.11和1.00±0.06。中、高剂量实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 HSYA可能通过抑制PI3K/Akt途径来减少中性粒细胞活性，从而抑制炎症反应，减轻肺损伤。
, authors=王忠芳
1, 吉自敏
2a, 林志强
2b, 李永兵
2a, 吕建华
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王忠芳（1980-），女，副主任护师，主要从事急危重症方向的相关工作
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