Article(id=1276976096847466600, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251011.704, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1756137600000, receivedDateStr=2025-08-26, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384426556, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384426556, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384426556, creator=13701087609, updateTime=1782384426556, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=472, endPage=481, ext={EN=ArticleExt(id=1276976097023627370, articleId=1276976096847466600, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Effects of Acanthopanax senticosus extract on Parkinson's disease mice via untargeted lipidomics across multiple brain regions, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study aimed to investigate the mechanisms by which Acanthopanax senticosus extract (ASH) exerts effects onα-synuclein (α-syn) overexpressing transgenic mouse model of Parkinson's disease (PD), with a focus on its regulation of brain lipid metabolism. Twenty PD model mice were randomly assigned to a model group or an ASH treatment group (45.5 mg·kg^-1 by gavage for 4 weeks), and 10 C57BL/6 mice served as a normal control group. Behavioral assessments revealed that, compared with controls, PD model mice showed prolonged pole test time, reduced spontaneous locomotor activity, shorter latency to fall in the rotarod test, and decreased total distance traveled in the open field test. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), caspase-9 were significantly elevated, B-cell lymphoma-2 (Bcl-2), and proliferating cell nuclear antigen (PCNA) expression was reduced, and marked neuronal damage was observed in brain tissue. ASH intervention significantly improved these behavioral and biochemical parameters and attenuated neuronal injury. Untargeted lipidomics analysis revealed significant alterations in sphingomyelin (SM), ceramide (Cer), phosphatidylcholine (PC), and phosphatidylserine (PS) across multiple brain regions (cortex, substantia nigra, cerebellum, and striatum) in PD mice, which were notably restored by ASH treatment. Pathway analysis indicated that these metabolites were predominantly involved in sphingolipid metabolism. Western blot further demonstrated that ASH downregulated the expression of key sphingolipid metabolic enzymes serine palmitoyltransferase long-chain base subunits 1 and 2 (SPTLC1 and SPTLC2) and upregulated UDP-glucose ceramide glucosyltransferase (UGCG), β-galactosylceramidase (GALC), and sphingosine kinase 2 (SPHK2), thereby suppressing abnormal SM and Cer accumulation in the substantia nigra and elevating PS and PC levels in the striatum. Spearman's correlation analysis supported the modulatory effect of ASH on brain lipid metabolic profiles. In conclusion, ASH improves behavioral deficits, exerts anti-inflammatory effects, and regulates sphingolipid metabolism to correct disordered lipid profiles, thereby providing neuroprotective effects in PD mice.

, authors=null, authorsList=Ao GAO, Xiao-min XU, Ning-xia LU, Dong-hua YU, Yu WANG, Ping-ping CHEN, Fang LU, Shu-min LIU, authorCompany=null, correspAuthors=Fang LU, Shu-min LIU, 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=1276976097229148268, articleId=1276976096847466600, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于多脑区非靶向脂质代谢组学的刺五加提取物对PD小鼠的作用研究, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

该研究旨在探讨刺五加提取物（ASH）对α-突触核蛋白（α-syn）过表达转基因帕金森病（PD）模型小鼠的作用机制，重点关注其对脑内脂质代谢的影响。将20只PD模型小鼠随机分为模型组和ASH组（45.5 mg·kg^-1灌胃，干预4周），并设10只C57BL/6小鼠为空白组。通过行为学测试发现，与空白组相比，模型组小鼠爬杆时间延长、自主活动减少、在棒时间缩短、旷场实验活动总距离缩短，血清中肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、天冬氨酸特异性的半胱氨酸蛋白水解酶-9 （caspase-9）水平显著升高，B淋巴细胞瘤-2（Bcl-2）和增殖细胞核抗原（PCNA）表达降低，脑组织出现明显神经元损伤。ASH干预后上述行为学指标和血清指标均得到显著改善，神经损伤减轻。非靶向脂质代谢组学分析显示，模型组小鼠脑内多个区域（皮层、黑质、小脑、纹状体）的鞘磷脂（SM）、神经酰胺（Cer）、磷脂酰胆碱（PC）、磷脂酰丝氨酸（PS）等脂质丰度发生显著变化，ASH干预后这些代谢物出现显著回调。通路分析表明这些代谢物共同参与鞘脂代谢通路。Western blot结果进一步显示，ASH能显著下调鞘脂代谢关键蛋白丝氨酸棕榈酰转移酶长链碱基亚基1和2（SPTLC1和SPTLC2）的表达，同时显著上调UDP-葡萄糖神经酰胺糖基转移酶（UGCG）、β-半乳糖脑苷酯酶（GALC）和鞘氨醇激酶2（SPHK2）的表达，从而抑制黑质区SM和Cer的异常蓄积，并提高纹状体区域PS和PC水平。Spearman相关性分析支持了ASH对脑组织代谢轮廓的调节作用。综上所述，ASH可以改善PD的行为学障碍，发挥抗炎作用，调控鞘脂代谢通路，改善脂质代谢紊乱，进而发挥对PD的神经保护作用。

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高澳，博士研究生，主要从事中药药性理论及药物功效研究，E-mail: 1453531667@qq.com

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高澳，博士研究生，主要从事中药药性理论及药物功效研究，E-mail: 1453531667@qq.com

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