Article(id=1276976083434074726, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250814.401, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753027200000, receivedDateStr=2025-07-21, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384423358, onlineDateStr=2026-06-25, pubDate=1767196800000, pubDateStr=2026-01-01, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384423358, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384423358, creator=13701087609, updateTime=1782384423358, updator=13701087609, issue=Issue{id=1276975955985961244, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='1', pageStart='1', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1767196800000', pubDateStr='2026-01-01', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1782384392973, creator='13701087609', updateTime=1782384484405, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976339546673871, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976339546673872, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=211, endPage=220, ext={EN=ArticleExt(id=1276976083870282344, articleId=1276976083434074726, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Baihe Dihuang Decoction attenuates hippocampal neuronal injury in anxious depression by inhibiting SHP2, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study explored the mechanism by which the classical prescription Baihe Dihuang Decoction alleviates neuronal injury in anxious depression, based on the Src homology 2 domain-containing protein tyrosine phosphatase (SHP2) signaling pathway. Sprague-Dawley rats were randomly divided into a normal group, model group, venlafaxine group (13.5 mg·kg^-1), and Baihe Dihuang Decoction high-, medium-, and low-dose groups (16, 8, and 4 g·kg^-1, respectively). An anxious depression model was established using 28 days of chronic restraint stress (6 h/day) combined with corticosterone administration (30 mg·kg^-1, ih). From day 8 of modeling, intragastric administration of the corresponding treatments was given for 21 consecutive days. Anxiety-and depression-like behaviors were evaluated. Golgi staining was used to observe dendritic spine morphology of hippocampal neurons, and Western blot was performed to detect hippocampal phosphorylated (p)-SHP2, synapsin 1 (SYN1), and postsynaptic density protein-95 (PSD-95). In cell experiments, primary hippocampal neurons were transfected with lentiviruses to specifically overexpress or knock down SHP2. Transfection efficiency was assessed by RT-PCR and Western blot. A corticosterone-induced neuronal injury model was established, followed by intervention with Baihe Dihuang Decoction-containing serum. Cell viability was measured using the MTT assay, apoptotic morphology was observed by Hoechst 33342 staining, apoptosis rates were determined via flow cytometry, and immunofluorescence was used to detect SHP2, p-SHP2, SYN1, and PSD-95 expression. The results showed that, compared with the normal group, model rats exhibited hippocampal dendritic spines with atrophy, loss, irregular morphology, and shortening, accompanied by significantly reduced SYN1 and PSD-95 expression and markedly increased p-SHP2/SHP2 levels. After Baihe Dihuang Decoction intervention, hippocampal neuronal injury was significantly alleviated, and p-SHP2/SHP2 levels were suppressed. In vitro, neuronal SHP2 overexpression (SHP2 OE) or corticosterone modeling led to a marked decrease in cell viability, increase in apoptosis rate, and downregulation of SYN1 and PSD-95. Following treatment with Baihe Dihuang Decoction-containing serum, SHP2 overexpression was inhibited, cell viability increased, apoptosis decreased, and SYN1 and PSD-95 expression significantly increased. In addition, SHP2 knockdown (SHP2 KD) via lentiviral transfection also mimicked the protective effects of Baihe Dihuang Decoction. In conclusion, Baihe Dihuang Decoction improves hippocampal neuronal injury in anxious depression by regulating the SHP2 signaling pathway.

, authors=null, authorsList=Jia-cheng DAI, Rong-lin CHEN, Ke-xin HE, Lin TANG, Pan MENG, Yu-hong WANG, Hong-qing ZHAO, authorCompany=null, correspAuthors=Hong-qing ZHAO, 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=1276976084365210218, articleId=1276976083434074726, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=百合地黄汤通过抑制SHP2改善焦虑性抑郁症海马神经元损伤, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

基于Src同源-2结构域蛋白酪氨酸磷酸酶（SHP2）信号探讨经典名方百合地黄汤改善焦虑性抑郁症神经元损伤机制。将SD大鼠随机分为正常组，模型组，文拉法辛组（13.5 mg·kg^-1），百合地黄汤高、中、低剂量组（16、8、4 g·kg^-1）。采用28 d慢性束缚应激（6 h）联合皮质酮（ih，30 mg·kg^-1）的方法建立焦虑性抑郁症大鼠模型，从造模第8天起连续灌胃给药21 d，评价焦虑和抑郁样行为；高尔基染色观察海马神经元树突棘形态变化，Western blot法检测海马磷酸化（p）-SHP2、突触蛋白1（SYN1）、突触后致密蛋白-95（PSD-95）表达。细胞实验中，通过慢病毒转染特异性过表达或敲低神经元SHP2表达，RT-PCR和Western blot法评价转染效率，皮质酮造模诱导神经元损伤并给予百合地黄汤含药血清干预。MTT法检测细胞存活率，Hoechst 33342染色检测细胞凋亡状态，流式细胞术检测细胞凋亡率，免疫荧光法检测SHP2、p-SHP2、SYN1、PSD95表达。结果显示，与正常组比较，模型组大鼠海马树突棘呈现萎缩、消失、形态不规则、短缩等特征，SYN1、PSD-95表达显著降低，p-SHP2/SHP2水平显著增加；百合地黄汤干预后，大鼠海马神经元损伤情况显著改善，p-SHP2/SHP2水平受到抑制。体外神经元成功转染SHP2过表达（SHP2 OE）病毒或经皮质酮造模后，细胞存活率显著下降，细胞凋亡率显著增加，SYN1、PSD-95表达均显著降低；百合地黄汤含药血清干预后，神经元SHP2高表达受到抑制，细胞存活率增加，凋亡减少，SYN1、PSD-95表达均显著增加；此外，转染SHP2干扰（SHP2 KD）慢病毒也能模拟百合地黄汤的保护作用。综上，百合地黄汤能够通过调控SHP2信号改善焦虑性抑郁症海马神经元损伤。

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戴佳程，硕士研究生，E-mail: 1371168137@qq.com

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