Article(id=1276976162337326006, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250915.701, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1756915200000, receivedDateStr=2025-09-04, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384442170, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384442170, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384442170, creator=13701087609, updateTime=1782384442170, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=482, endPage=492, ext={EN=ArticleExt(id=1276976162517681080, articleId=1276976162337326006, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Mechanisms of Periplaneta americana extract in regulating JAK1/PI3K/AKT signaling pathway to intervene in patient-derived early-stage lung adenocarcinoma organoids with ground-glass nodule features, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study aimed to elucidate the therapeutic effects and molecular mechanisms of Periplaneta americana extract (PAE) on ground-glass nodule (GGN) -type early-stage lung adenocarcinoma (LUAD) using patient-derived organoid (PDO) models. GGN-type patient-derived early-stage LUAD organoid (GGN-PDO) were successfully established. At the level of drug quality control and component analysis, the content of free amino acids and peptides in PAE were determined by high-performance liquid chromatography (HPLC), and the main components were further analyzed by liquid chromatography-mass spectrometry (LC-MS). Analysis of variance was used to evaluate the similarity between drugs of the same batch (Pearson correlation coefficient 0.87-0.99) and ensure quality control. At the histopathological level, hematoxylin-eosin (HE) staining and immunohistochemical (IHC) analysis of key molecular markers, including cytokeratin 7 (CK7), thyroid transcription factor-1 (TTF-1), and Ki-67, confirmed that the organoids recapitulated the tumor characteristics of parental tissues. Pharmacodynamic evaluation demonstrated that PAE significantly inhibited the proliferation and viability of GGN-PDOs in a dose-dependent manner, while immunofluorescence (IF) staining showed a marked reduction in the proliferation marker Ki-67. Flow cytometry further confirmed that PAE induced apoptosis in GGN-PDO, and Western blot analysis demonstrated that PAE downregulated the anti-apoptotic protein Bcl-2 and upregulated the pro-apoptotic protein Bax, thereby activating the apoptotic pathway. Notably, for the first time, the pro-apoptotic mechanism of PAE was shown to involve inhibition of the Janus kinase 1 (JAK1)/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, as evidenced by markedly decreased protein levels of JAK1, PI3K, p-PI3K, AKT, and p-AKT following PAE treatment. In summary, this study is the first to use a clinically relevant GGN-PDO models to demonstrate that PAE induces apoptosis in early-stage LUAD via JAK1/PI3K/AKT pathway inhibition, providing a solid theoretical and experimental basis for developing innovative pharmacotherapies and non-surgical interventions against GGNs.

, authors=null, authorsList=Jia-wei HE, Chun-xia HUANG, Yang ZHONG, Qiong MA, Jia LI, Heng-zhou LAI, Ping XIAO, Yi-feng REN, Fu-neng GENG, Tao-qing WU, Yi-fang JIANG, Xue-ke LI, Feng-ming YOU, Xi FU, authorCompany=null, correspAuthors=Feng-ming YOU, Xi FU, 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=1276976162739979194, articleId=1276976162337326006, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=美洲大蠊提取物调控JAK1/PI3K/AKT信号通路干预磨玻璃结节型患者源性早期肺腺癌类器官的机制研究, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

该研究旨在利用患者源性类器官（PDO）模型，阐明传统中药美洲大蠊提取物（PAE）对磨玻璃结节（GGN）型早期肺腺癌的干预作用及分子机制，成功构建了GGN型患者源性早期肺腺癌类器官（GGN-PDO）模型。药品质控及成分鉴定层面，利用高效液相色谱（HPLC）对PAE游离氨基酸与肽类含量进行测定，进一步采用液相色谱-质谱联用（LC-MS）对PAE主要成分进行解析，并应用方差分析评估同一批次药品间的相似性（皮尔逊相关系数范围0.87～0.99）并实现质量控制。组织病理学层面，苏木素-伊红（HE）染色及关键分子标志物细胞角蛋白7（CK7）、甲状腺转录因子-1（TTF-1）、增殖细胞核抗原（Ki-67）的免疫组化（IHC）染色均表征了类器官的肿瘤组织特征。药效学评价显示，PAE能以剂量依赖方式显著抑制GGN-PDO的增殖及细胞活力，同时免疫荧光（IF）染色表明PAE处理可显著降低细胞增殖核心指标Ki-67的表达水平。流式细胞术定量分析证实PAE可显著诱导GGN-PDO细胞凋亡，且Western blot分析进一步确证了PAE处理可下调抗凋亡蛋白B细胞淋巴瘤/白血病-2基因（Bcl-2）的表达，上调促凋亡蛋白Bcl-2相关X蛋白（Bax）的表达，从而激活凋亡通路。尤为关键的是，首次发现PAE促进细胞凋亡的作用机制与抑制Janus激酶1（JAK1）/磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）信号通路有关，表现为PAE干预后显著降低JAK1、PI3K、p-PI3K、AKT及p-AKT蛋白水平。综上，该研究首次利用与临床高度相关的GGN-PDO模型揭示PAE通过抑制JAK1/PI3K/AKT信号通路诱导早期肺腺癌细胞凋亡，为开发针对GGN的创新药物及非手术干预策略奠定了重要的理论与实验基础。

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