Article(id=1322901694861947282, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322901641049015115, articleNumber=null, orderNo=null, doi=null, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=1616601600000, acceptedDateStr=2021-03-25, onlineDate=1793333942377, onlineDateStr=2026-10-30, pubDate=1626278400000, pubDateStr=2021-07-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793333942377, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793333942377, creator=13701087609, updateTime=1793333942377, updator=13701087609, issue=Issue{id=1322901641049015115, tenantId=1146029695717560320, journalId=1235980733773295621, year='2021', volume='30', issue='13', pageStart='1153', pageEnd='1248', issueExtLink='null', onlineDate='null', pubDate='1626278400000', pubDateStr='2021-07-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1793333929460, creator='13701087609', updateTime=1793333989426, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322901892623376986, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322901641049015115, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322901892627571291, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322901641049015115, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1168, endPage=1175, ext={EN=ArticleExt(id=1322901695671447955, articleId=1322901694861947282, tenantId=1146029695717560320, journalId=1235980733773295621, language=EN, title=The hepatocarcinogenic effects of aristolochic acid I and associated mechanisms in C3H/HeN suckling mice, columnId=null, journalTitle=Chinese Journal of New Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: To explore the potential hepatocarcinogenic effect of aristolochic acid I (AAI) on 2-week-old C3H/HeN suckling mice and its possible mechanism.
Methods: Two-week-old C3H/HeN suckling mice were randomly divided into 3 groups, i.e., the vehicle control group (0.5% CMC-Na), the liver cancer positive agent model group (DEN 20 mg·kg-1) and the AAI group (AAI 10 mg·kg-1). After 9 months of observation after a single administration, the organs were taken for gross pathological and histopathological examination, and the levels of serum biochemical indicators such as ALT, AST and AFP in mice were detected. At the same time, the contents of IL-1β and IL-6, the expression of Ki67, CK19, NF-κB P65, Ras, Raf, and caspase-3 in mouse liver were detected.
Results: In this experiment, AAI caused liver cancer in C3H/HeN suckling mice. The incidence of liver cancer in male and female mice were 78.57% and 41.67%, respectively. Compared with the vehicle control group, the levels of ALT, AST, AFP, IL-1β and IL-6 in the AAI group were significantly increased, and the expression of Ki67 and CK19 in liver were positive. The results of Western blot showed that AAI significantly increased the expression of NF-κB P65, P-AKT, Ras, C-Jun, C-Fos, C-MYC and Bcl-2, and significantly decreased the expression of IKBα, Bax and Caspase-3.
Conclusion: In this experiment, AAI caused liver cancer in 2-week-old C3H/HeN suckling mice. The mechanism may be related to the activation of PI3K/AKT inflammatory pathway in hepatocytes, Ras/AP1/C-MYC proliferation pathway and the inhibition of Bax/Bcl-2/Caspase-3 Mitochondrial apoptosis pathway.
, authors=Ting WANG
1, Wen-xiao WU
1, 2, Zhi LIN
1, Chao WANG
1, Yan-wei YANG
1, Yu-fa MIAO
1, Xing-chao GENG
1, Bo LI
3, authorsList=Ting WANG, Wen-xiao WU, Zhi LIN, Chao WANG, Yan-wei YANG, Yu-fa MIAO, Xing-chao GENG, Bo LI, authorCompany=null, correspAuthors=Xing-chao GENG, Bo LI, 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=1322901696820687252, articleId=1322901694861947282, tenantId=1146029695717560320, journalId=1235980733773295621, language=CN, title=马兜铃酸I致C3H/HeN乳鼠肝癌及机制探索, columnId=1236331161786569054, journalTitle=中国新药杂志, columnName=重大新药创制专项巡礼, runingTitle=null, highlight=null, articleAbstract=
目的： 探索马兜铃酸I（aristolochic acid I，AAI）对2周龄C3H/HeN乳鼠的潜在致肝癌作用及其可能的作用机制。
方法： 将2周龄的C3H/HeN乳鼠雌雄各半随机分为3组，溶媒对照组（0.5% CMC-Na），阳性剂对照组（DEN 20 mg·kg-1）和AAI组（AAI 10 mg·kg-1）。单次给药后观察9个月，取各脏器进行大体病理学和组织病理学检查，同时检测小鼠血清中谷丙转氨酶（ALT）、谷草转氨酶（AST）等血清生化指标水平和甲胎蛋白（AFP）含量，肝脏中白细胞介素IL-1β和IL-6含量，Ki67蛋白和细胞角质蛋白19（CK19）的表达，NFκB P65，Ras/Raf，Caspase-3等蛋白表达水平。
结果： 在本实验条件下，单次灌胃给予AAI可导致C3H/HeN乳鼠发生肝癌，雄性、雌性小鼠肝癌的发生率分别为78.57%和41.67%。与溶媒对照组相比，AAI组小鼠体内ALT，AST，AFP，IL-1β和IL-6水平显著升高，肝脏Ki67和CK19表达呈阳性，NFκB P65，P-AKT，Ras，C-Jun，C-Fos，C-MYC和Bcl-2表达显著升高，IKBα，Bax和Caspase-3表达显著降低。
结论： 本实验条件下，AAI可以引起2周龄C3H/HeN乳鼠发生肝脏肿瘤，其机制可能与激活肝细胞内PI3K/AKT炎症通路、Ras/AP1/C-MYC促增殖通路和抑制Bax/Bcl-2/Caspase-3线粒体凋亡通路有关。
, authors=王婷
1, 吴文晓
1, 2, 林志
1, 王超
1, 杨艳伟
1, 苗玉发
1, 耿兴超
1, 李波
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王婷，女，硕士研究生，研究方向：药物临床前安全性评价。联系电话：（010）67872233，E-mail：15011437476@163.com。
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