Article(id=1321425895349403796, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425847911830056, articleNumber=null, orderNo=null, doi=10.20251/j.cnki.1003-3734.2026.17.005, 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=1779724800000, acceptedDateStr=2026-05-26, onlineDate=1792982084357, onlineDateStr=2026-10-26, pubDate=1789401600000, pubDateStr=2026-09-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792982084357, onlineIssueDateStr=2026-10-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792982084357, creator=13701087609, updateTime=1792982084357, updator=13701087609, issue=Issue{id=1321425847911830056, tenantId=1146029695717560320, journalId=1235980733773295621, year='2026', volume='35', issue='17', pageStart='1793', pageEnd='1904', issueExtLink='null', onlineDate='null', pubDate='1789401600000', pubDateStr='2026-09-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792982073047, creator='13701087609', updateTime=1792982858328, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1321429141673586821, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425847911830056, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1321429141673586822, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425847911830056, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1822, endPage=1827, ext={EN=ArticleExt(id=1321425895517175957, articleId=1321425895349403796, tenantId=1146029695717560320, journalId=1235980733773295621, language=EN, title=Multi-target antidepressant mechanism of Shenge Bushen Capsules, columnId=null, journalTitle=Chinese Journal of New Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: To systematically explore the antidepressant multi-target mechanism of Shenge Bushen Capsules, and evaluate its direct effect on dopamine (DA) and norepinephrine (NE) system, as well as the inhibition of monoamine oxidase A (MAO-A) activity and the protective effect on glucose-deficient and hypoxic neurons.
Methods: The effects of yohimbine on DA and NE systems were evaluated by apomorphine-induced mouse stereotyped behavior model and yohimbine-enhanced toxicity test, respectively. Its effect on MAO-A activity in mouse brain was studied by in vitro fluorescence assay. The model of oxygen-glucose deprivation injury was established by primary cultured mouse cortical neurons, and the neuroprotective activity was evaluated by detecting the leakage rate of lactate dehydrogenase (LDH).
Results: Shenge Bushen Capsules had no significant effect on apomorphine-induced stereotyped behavior and did not enhance the lethal toxicity of yohimbine. In vitro experiments showed that the drug had a significant inhibitory effect on MAO-A at a concentration of 4×10-4 g·mL-1. In the neuroprotective experiment, Shenge Bushen Capsules could significantly reduce the LDH leakage rate of glucose-deficient hypoxic neurons at a low concentration of 10×10-6 g·mL-1 in a concentration-dependent manner.
Conclusion: The antidepressant effect of Shenge Bushen Capsules is not achieved by directly regulating the DA or NE system. The mechanism is related to the inhibition of MAO-A activity to reduce the degradation of monoamine neurotransmitters and the direct protection of neurons from damage.
, authors=Chang-bing PU
1, Hui-juan DONG
2, Juan HAO
3, Shi-xian HU
1, Bin REN
1, Chao-jun YANG
1, *, authorsList=Chang-bing PU, Hui-juan DONG, Juan HAO, Shi-xian HU, Bin REN, Chao-jun YANG, authorCompany=null, correspAuthors=Chao-jun YANG, 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=1321425895936606358, articleId=1321425895349403796, tenantId=1146029695717560320, journalId=1235980733773295621, language=CN, title=参葛补肾胶囊的多靶点抗抑郁机制研究, 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: 系统探究参葛补肾胶囊的多靶点抗抑郁作用机制,重点评估其对多巴胺(dopamine, DA)、去甲肾上腺素(norepinephrine, NE)系统的直接影响以及对脑单胺氧化酶A(monoamine oxidase A, MAO-A)活性的抑制和对缺糖缺氧神经元的保护作用。
方法: 采用阿扑吗啡诱导的小鼠刻板行为模型和育亨宾增强毒性实验分别评价其对DA和NE系统的作用;通过体外荧光测定法研究其对小鼠脑MAO-A活性的影响;利用原代培养小鼠皮层神经元建立缺糖缺氧损伤模型,通过检测乳酸脱氢酶(lactate dehydrogenase, LDH)逸漏率评估其神经保护活性。
结果: 参葛补肾胶囊对阿扑吗啡诱导的小鼠刻板行为无显著影响,且不增强育亨宾的致死毒性。体外实验表明,该药在4×10-4 g·mL-1浓度下对MAO-A具有显著抑制作用。在神经保护实验中,参葛补肾胶囊在10×10-6 g·mL-1的低浓度下即能显著降低缺糖缺氧神经元的LDH逸漏率,并呈浓度依赖性。
结论: 参葛补肾胶囊的抗抑郁作用并非通过直接调控DA或NE系统实现,其机制与抑制MAO-A活性以减少单胺类神经递质降解以及直接保护神经元免受损伤等多靶点协同作用有关。
, authors=蒲长兵
1, 董惠娟
2, 郝娟
3, 胡时先
1, 任宾
1, 杨朝竣
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