Article(id=1291404897694503667, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404791758975909, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.11.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1734624000000, receivedDateStr=2024-12-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824520752, onlineDateStr=2026-08-04, pubDate=1750089600000, pubDateStr=2025-06-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824520752, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824520752, creator=13701087609, updateTime=1785824520752, updator=13701087609, issue=Issue{id=1291404791758975909, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='11', pageStart='1501', pageEnd='1650', issueExtLink='null', onlineDate='null', pubDate='1750089600000', pubDateStr='2025-06-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824495496, creator='13701087609', updateTime=1785824495496, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1582, endPage=1588, ext={EN=ArticleExt(id=1291404898348815092, articleId=1291404897694503667, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Study on the gastric protective effects of salvianolic acid B on gastric precancerous lesions in rats by regulating the
miR-106
b-5
p/BTG3 molecular axis, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the specific mechanism of the gastric protective effect of salvianolic acid B (Sal B) on precancerous lesions of the stomach (PLGC) in rats by regulating the microRNA (miR)-106b-5p/B-cell translocation gene 3 (BTG3) molecular axis.
Methods Except for the NC group, the rat models of PLGC were established. The rats were randomly divided into the NC group (without any treatment, intragastric administration of normal saline), the model group (after successful modeling, intragastric administration of normal saline), the experimental group (intragastric administration of Sal B based on the model group), the NC mimic group (based on the experimental group, injection of NC mimic plasmid via the tail vein), the miR-106b-5p mimic group (based on the experimental group, injection of miR-106b-5p mimic plasmid via the tail vein), the pcDNA3.1-NC group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-NC plasmid) and the pcDNA3.1-BTG3 group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-BTG3 plasmid). Quantitative real-time polymerase chain reaction experiments were carried out to detect the mRNA expression levels of miR-106b-5p, BTG3 and inflammatory factors in the gastric mucosa tissues. Enzyme-linked immunosorbent assays were performed to detect the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and gastrin-17 (G-17) in the serum. Western blot experiments were used to detect the levels of proteins related to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and mucin 2 (MUC2) in the gastric mucosa tissues.
Results The relative expression levels of miR-106b-5p in the NC group, the model group and the experimental group were 1.00±0.08, 1.76±0.35 and 1.33±0.26, respectively, and the relative expression levels of BTG3 mRNA were 1.00±0.05, 0.39±0.06 and 0.81±0.15, respectively. There were statistically significant differences in the above-mentioned indicators between the model group and the NC group, as well as between the experimental group and the model group (all P<0.05). The levels of SOD in the NC group, the model group, the experimental group, the NC mimic group, the miR-106b-5p mimic group, the pcDNA3.1-NC group and the pcDNA3.1-BTG3 group were (197.81±47.15), (118.54±20.49), (172.29±34.34), (176.78±35.57), (127.65±21.23), (119.41±20.50) and (158.28±31.07) U·mL-1, respectively; the levels of MDA were (3.44±0.67), (8.08±1.32), (3.92±0.75), (3.84±0.70), (6.50±1.21), (6.34±1.17) and (4.22±0.79) nmol·mL-1, respectively; the levels of G-17 were (221.57±40.26), (155.62±28.43), (201.13±37.35), (194.85±35.24), (162.72±31.65), (160.04±29.37) and (189.32±32.15) pg·mL-1, respectively; the levels of PI3K were 1.00±0.14, 1.81±0.36, 1.23±0.21, 1.19±0.20, 1.65±0.32, 1.70±0.35 and 1.38±0.28, respectively; the ratios of phosphorylated AKT/AKT were 1.00±0.09, 1.94±0.39, 1.27±0.23, 1.21±0.18, 1.77±0.37, 1.73±0.33 and 1.42±0.26, respectively. There were statistically significant differences in the above-mentioned indicators between the miR-106b-5p mimic group and the NC mimic group, and between the pcDNA3.1-BTG3 group and the pcDNA3.1-NC group (all P<0.05).
Conclusion Sal B may exert a gastric protective effect by down-regulating the targeted negative regulation of BTG3 expression by miR-106b-5p, inhibiting the activation of the PI3K/AKT signaling pathway, thereby alleviating the oxidative stress and inflammatory response in PLGC rats and improving the condition of the gastric mucosa.
, authors=Jing HUANG, Ya-qiong LI, Xiao-hua JIANG, Yun-qin SUN, Tao LIU, authorsList=Jing HUANG, Ya-qiong LI, Xiao-hua JIANG, Yun-qin SUN, Tao LIU, authorCompany=null, correspAuthors=Jing HUANG, 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=1291404899791655669, articleId=1291404897694503667, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=丹酚酸B调控
miR-106
b-5
p/BTG3分子轴对大鼠胃癌前病变的胃保护作用研究, 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 探讨丹酚酸B（Sal B）调控微小RNA（miR）-106b-5p/B细胞易位基因3（BTG3）分子轴对大鼠胃癌前病变（PLGC）的胃保护作用的具体机制。
方法 除NC组外，其余各组建立PLGC大鼠模型。将大鼠随机分为NC组（不做任何处理，0.9% NaCl灌胃）、模型组（造模成功后，0.9% NaCl灌胃）、实验组（基于模型组，Sal B灌胃）、NC mimic组（基于实验组，尾静脉注射NC mimic质粒）和miR-106b-5p mimic组（基于实验组，尾静脉注射miR-106b-5p mimic质粒）、pcDNA3.1-NC组（基于miR-106b-5p mimic组，腹腔注射pcDNA3.1-NC质粒）和pcDNA3.1-BTG3组（基于miR-106b-5p mimic组，腹腔注射pcDNA3.1-BTG3质粒）。用实时荧光定量聚合酶链反应检测胃黏膜组织miR-106b-5p、BTG3及炎症因子mRNA表达水平；用酶联免疫吸附试验检测血清中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）和胃泌素-17（G-17）水平；用蛋白质印迹法检测胃黏膜组织中磷脂酰肌醇-3-激酶（PI3K）/蛋白激酶B（AKT）信号通路相关蛋白和黏蛋白2（MUC2）的表达水平。
结果 NC组、模型组和实验组miR-106b-5p相对表达水平分别为1.00±0.08、1.76±0.35和1.33±0.26，BTG3 mRNA相对表达水平分别为1.00±0.05、0.39±0.06和0.81±0.15。模型组的上述指标与NC组比较、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）；NC组、模型组、实验组、NC mimic组、miR-106b-5p mimic组、pcDNA3.1-NC组和pcDNA3.1-BTG3组SOD水平分别为（197.81±47.15）、（118.54±20.49）、（172.29±34.34）、（176.78±35.57）、（127.65±21.23）、（119.41±20.50）和（158.28±31.07）U·mL-1，MDA水平分别为（3.44±0.67）、（8.08±1.32）、（3.92±0.75）、（3.84±0.70）、（6.50±1.21）、（6.34±1.17）和（4.22±0.79）nmol·mL-1，G-17水平分别为（221.57±40.26）、（155.62±28.43）、（201.13±37.35）、（194.85±35.24）、（162.72±31.65）、（160.04±29.37）和（189.32±32.15）pg·mL-1，PI3K蛋白相对表达水平分别为1.00±0.14、1.81±0.36、1.23±0.21、1.19±0.20、1.65±0.32、1.70±0.35和1.38±0.28，磷酸化AKT/AKT分别为1.00±0.09、1.94±0.39、1.27±0.23、1.21±0.18、1.77±0.37、1.73±0.33和1.42±0.26。miR-106b-5p mimic组的上述指标与NC mimic组比较，pcDNA3.1-BTG3组的上述指标与pcDNA3.1-NC组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 Sal B可能通过下调miR-106b-5p靶向负调控BTG3表达，从而抑制PI3K/AKT信号通路的激活来减轻PLGC大鼠氧化应激与炎症反应，改善胃黏膜状况，从而发挥胃保护作用。
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黄静（1977-），女，硕士，讲师，主要从事消化内科方面的研究工作
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