Article(id=1317125535218643845, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.02.020, 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=null, acceptedDateStr=null, onlineDate=1791956798605, onlineDateStr=2026-10-14, pubDate=1770652800000, pubDateStr=2026-02-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791956798605, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791956798604, creator=13701087609, updateTime=1791956798604, updator=13701087609, issue=Issue{id=1317125500041015883, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='2', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1770652800000', pubDateStr='2026-02-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791956790217, creator='13701087609', updateTime=1791958795145, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133909368877755, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133909373072060, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=111, endPage=115, ext={EN=ArticleExt(id=1317125535419970438, articleId=1317125535218643845, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Effects of Drug-Containing Serum of Haipiaoxiao（Cuttlebone）on Proliferation and Angiogenesis of HUVEC Induced by High Glucose, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To observe the effect of Haipiaoxiao（Cuttlebone）drug-containing serum regulating PI3K/Akt/eNOS signaling pathway on proliferation，apoptosis and angiogenesis of vascular endothelial cells（HUVECs）induced by high glucose.
Method Twenty SD rats were selected，10 rats were randomly gavaged with Haipiaoxiao（Cuttlebone）water decoction and 10 rats with the same amount of normal saline. The corresponding serum was prepared 2 h after the last administration. HUVECs were cultured in vitro，the optimal high glucose concentration was screened，and the cells were induced for 24 h to establish a high glucose damage model. According to the induction conditions，they were divided into blank Control group，Model group，Haipiaoxiao（Cuttlebone）low group，Haipiaoxiao（Cuttlebone）medium group group，Haipiaoxiao（Cuttlebone）high group，and the corresponding serum was treated for 24 h. The cell proliferation was detected by CCK-8 method. Cell migration ability was evaluated by cell scratch assay. The apoptosis of cells in each group was detected by flow cytometry. Angiogenesis of each group was detected by in vitro tube formation. Real-time fluorescence quantitative polymerase chain reaction（qRT-PCR）was used to determine the mRNA expression of each group. The expressions of phosphatidylinositol 3-kinase（PI3K），p-PI3K，protein kinase B（Akt），p-Akt，endothelial nitric oxide synthase（eNOS）and human tumor suppressor gene（p53）protein were detected by Western blot.
Result The optimal concentration of high glucose induced endothelial cell injury was 30 mmol/L. Compared with those of the Control group，the cell activity，wound-healing rate，the number of angiogenesis experiment in vitro were decreased，the apoptosis rate and p53 protein expression were increased，the protein expressions of p-PI3K，p-Akt and eNOS were decreased，and mRNA expressions of PI3K，Akt and eNOS were decreased in the Model group. The differences were statistically significant（P<0.05）. Compared with the Model group，Haipiaoxiao（Cuttlebone）low，medium and high dose groups increased the cell survival rate，improved the wound-healing rate，increased the number of angiogenesis experiment，decreased the apoptosis rate and p53 protein expression，increased the protein expressions of p-PI3K，p-Akt and eNOS and the mRNA expressions of PI3K，Akt and eNOS. The differences were statistically significant（P<0.05）.
Conclusion Haipiaoxiao（Cuttlebone）drug-containing serum can mediate PI3K/Akt/eNOS signaling pathway to promote the proliferation，migration and angiogenesis of vascular endothelial cells.
, authors=Guowei WANG
1, Tao ZHUO
1, Sixian WU
1, Quanwei ZHENG
1, Mengying LI
2, Jiehui LI
3, Jianhang LIU
2, authorsList=Guowei WANG, Tao ZHUO, Sixian WU, Quanwei ZHENG, Mengying LI, Jiehui LI, Jianhang LIU, authorCompany=null, correspAuthors=null, 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=1317125535696794503, articleId=1317125535218643845, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=海螵蛸含药血清对高糖诱导的血管内皮细胞增殖及血管生成的影响, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 探究海螵蛸含药血清调控PI3K/Akt/eNOS信号通路对高糖诱导血管内皮细胞（HUVECs）增殖、凋亡及血管生成的影响。
方法 选取20只SD大鼠，随机对10只大鼠灌胃海螵蛸水煎剂，10只灌胃等量生理盐水，末次给药后2 h制备相应血清。体外培养HUVECs，筛选最佳造模高糖浓度，对细胞诱导24 h，建立高糖损伤模型。根据诱导情况分为空白对照组（Control组）、模型组（Model组）、海螵蛸低剂量组（CLG组）、海螵蛸中剂量组（CMG组）、海螵蛸高剂量组（CHG组），相应血清干预24 h。采用CCK-8法检测各组细胞增殖情况；细胞划痕实验评估各组细胞的迁移能力；流式细胞术检测各组细胞的凋亡情况；体外成管实验检测各组血管生成情况；采用实时荧光定量聚合酶链反应（qRT-PCR）测定各组细胞mRNA表达；采用蛋白免疫印迹法检测磷脂酰肌醇3-激酶（PI3K）、p-PI3K、蛋白激酶B（Akt）、p-Akt、内皮型一氧化氮合酶（eNOS）、人体抑癌基因（p53）蛋白表达情况。
结果 高糖诱导内皮细胞损伤的最佳浓度为30 mmol/L；与Control组比较，Model组细胞活性下降，划痕愈合率降低，体外成管数量减少，凋亡率及p53蛋白表达升高，p-PI3K、p-Akt、eNOS蛋白表达降低，PI3K、Akt、eNOS mRNA表达降低，差异均有统计学意义（P<0.05）；与Model组对比，CLG、CMG、CHG组细胞存活率上升，划痕愈合率提高，体外成管数量增加，凋亡率及p53蛋白表达下降，p-PI3K、p-Akt、eNOS蛋白表达及PI3K、Akt、eNOS mRNA表达均升高，差异均有统计学意义（P<0.05）。
结论 海螵蛸含药血清可介导PI3K/Akt/eNOS信号通路，从而促进血管内皮细胞的增殖、迁移及血管生成。
, authors=王国威
1, 卓涛
1, 吴思贤
1, 郑全伟
1, 李梦颖
2, 李杰辉
3, 刘建航
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