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Article(id=1322926921641763270, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.10.033, 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=1793339956912, onlineDateStr=2026-10-30, pubDate=1760025600000, pubDateStr=2025-10-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793339956912, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793339956912, creator=13701087609, updateTime=1793339956912, updator=13701087609, issue=Issue{id=1322926740955341011, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='10', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1760025600000', pubDateStr='2025-10-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793339913834, creator='13701087609', updateTime=1793340753123, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322930261259846420, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322930261259846421, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=176, endPage=181, ext={EN=ArticleExt(id=1322926923185267143, articleId=1322926921641763270, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Effects of Chaihu Shugan Powder（柴胡疏肝散）on AMPK/mTOR/ULK1 Pathway and Glial Gells in Depression Model Rats, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective

To investigate the regulatory effects of Chaihu Shugan Powder（柴胡疏肝散）on the adenylate-activated protein activating enzyme（AMPK）/mammalian target of rapamycin（mTOR）/UNC-51-like kinase 1（ULK1）pathway and glial cells in the orbitofrontal cortex（OFC）of depression model rats.

Methods

The rat model of depression was established by chronic unpredictable mild stress（CUMS）.According to the random number table，10 rats were selected as the normal group and 50 rats with successful modeling were divided into model group，escitalopram group（10.50 mg/kg），Chaihu Shugan Powder lowdose group（3.15 g/kg），Chaihu Shugan Powder middle-dose group（6.30 g/kg），Chaihu Shugan Powder high-dose group（12.60 g/kg）according to the random number table，with ten rats in each group for 28 consecutive days.The changes of sugar preference coefficient，suspension immobility time and open field walking distance of rats in each group were observed.After the above detection was completed，the head was decapitated and the brain was removed，and the expressions of ionized calciumbinding receptor molecule 1（Iba-1），myelin basic protein（MBP）and glial fibrillary acidic protein（GFAP）in rat OFC tissues were detected by immunofluorescence assay.Western blotting method was used to detect the protein expressions of pT172-AMPK/AMPK，pS2488-mTOR/mTOR and pS757-ULK1/ULK1 in OFC tissue.The expressions of AMPK，mTOR and ULK1 mRNA in OFC were detected by real-time PCR.

Results

Compared to the control group，the model group and each treatment group showed a decrease in sucrose preference coefficient，an increase in immobility time in the forced swimming test and a decrease in distance traveled in the open field test（P<0.05，P<0.01）.Compared to the model group，each treatment group showed an increase in sucrose preference coefficient，a decrease in immobility time and an increase in distance traveled in the open field test（P<0.01）.Compared to the control group，the model group and each treatment group showed an increase in protein expressions of Iba-1 and GFAP（P<0.05，P<0.01），and a decrease in MBP protein expression（P<0.01），except those in the Chaihu Shugan Powder low-dose group.Compared to the model group，each treatment group showed a decrease in protein expressions of Iba-1 and GFAP（P<0.01），and an increase in MBP protein expression（P<0.01）.Compared to the control group，the model group and each treatment group showed a decrease in protein expressions of pT172-AMPK/AMPK，pS2448-mTOR/mTOR and pS757-ULK1/ULK1（P<0.05，P<0.01）.Compared to the model group，each treatment group showed an increase in protein expressions of pT172-AMPK/AMPK，pS2448-mTOR/mTOR and pS757-ULK1/ULK1（P<0.05）.Compared to the control group，the model group，escitalopram group，Chaihu Shugan Powder low-dose group and middle-dose group showed a decrease in expressions of mTOR and ULK1 mRNA（P<0.01），Chaihu Shugan Powder low-dose group showed a decrease in AMPK mRNA expression（P<0.05），and the Chaihu Shugan Powder high-dose group group showed a decrease in mTOR mRNA expression（P<0.01）.Compared to the model group，each treatment group showed an increase in expressions of AMPK mRNA，mTOR mRNA nd ULK1 mRNA（P<0.01）.

Conclusion

Chaihu Shugan Powder can reduce the expressions of Iba-1 and GFAP in OFC of rats，increase the expression of MBPand activate AMPK/mTOR/ULK1 pathway expression to exert the antidepressant effect.

, authors=Ming CHENG, Feng CAO, Zhen ZHANG, authorsList=Ming CHENG, Feng CAO, Zhen ZHANG, authorCompany=null, correspAuthors=Zhen ZHANG, 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=1322926925064315354, articleId=1322926921641763270, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=柴胡疏肝散对抑郁症模型大鼠AMPK/mTOR/ULK1通路及胶质细胞的作用, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的

探讨柴胡疏肝散对抑郁症模型大鼠眶额皮层（OFC）腺苷酸活化蛋白激活酶（AMPK）/哺乳动物雷帕霉素靶蛋白（mTOR）/UNC-51样激酶1（ULK1）通路及胶质细胞的调控作用。

方法

采用慢性不可预测轻度应激（CUMS）法制备抑郁症大鼠模型。按照随机数字表法选取10只大鼠作为正常组，将造模成功的50只大鼠按随机数字表法分为模型组、艾司西酞普兰组（10.50 mg/kg）、柴胡疏肝散低剂量组（3.15 g/kg）、柴胡疏肝散中剂量组（6.30 g/kg）、柴胡疏肝散高剂量组（12.60 g/kg），每组10只，连续灌胃28 d。观察各组大鼠糖水偏好系数、悬浮不动时间、旷场行走路程的变化。待上述检测完成后断头取脑，采用免疫荧光法检测大鼠OFC中离子钙结合受体分子1（Iba-1）、髓鞘碱性蛋白（MBP）、胶质纤维酸性蛋白（GFAP）的表达；Western blotting法检测OFC中pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的蛋白表达；实时荧光PCR法检测OFC中AMPK、mTOR、ULK1 mRNA的表达。

结果

与正常组比较，模型组及各给药组糖水偏好系数降低、悬浮不动时间增加、旷场行走路程减少（P<0.05，P<0.01）；与模型组比较，各给药组的糖水偏好系数升高、悬浮不动时间减少、旷场行走路程均有所升高（P<0.01）；与正常组比较，Iba-1及GFAP除柴胡疏肝散高剂量组外，模型组及各给药组Iba-1及GFAP均升高（P<0.05，P<0.01），MBP均降低（P<0.01）；与模型组比较，各给药组Iba-1、GFAP均降低（P<0.01）、MBP均升高（P<0.01）；与正常组比较，模型组及各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR及pS757-ULK1/ULK1蛋白表达均降低（P<0.05，P<0.01）；与模型组比较，各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR、pS757-ULK1/ULK1蛋白表达均升高（P<0.05）；与正常组比较，模型组、艾司西酞普兰组及柴胡疏肝散低、中剂量组mTOR、ULK1 mRNA表达均降低（P<0.01），柴胡疏肝散低剂量组的AMPK mRNA、柴胡疏肝散低、高剂量组的mTOR mRNA表达降低（P<0.05，P<0.01）；与模型组比较，各给药组AMPK mRNA、mTOR mRNA、ULK1 mRNA表达均升高（P<0.01）。

结论

柴胡疏肝散可以通过降低大鼠OFC组织中Iba-1、GFAP，升高MBP的表达，激活AMPK/mTOR/ULK1通路以发挥其抗抑郁作用。

, authors=程茗, 曹峰, 张震, authorsList=程茗, 曹峰, 张震, authorCompany=null, correspAuthors=张震, authorNote=

程茗（1999-），女，山东烟台人，硕士在读，研究方向：中医情志病防治。

, correspAuthorsNote=
张震（1987-），男，山东潍坊人，副教授，硕士研究生导师，博士，博士后，研究方向：中医肝藏象情志致病。E-mail：。
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程茗（1999-），女，山东烟台人，硕士在读，研究方向：中医情志病防治。

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程茗（1999-），女，山东烟台人，硕士在读，研究方向：中医情志病防治。

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Biomolecules，2022，12（11）：1587., articleTitle=Fine-tuning of mTORC1-ULK1-PP2A regulatory triangle is crucial for robust autophagic response upon cellular stress, refAbstract=null), Reference(id=1322926934673465901, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, doi=null, pmid=null, pmcid=null, year=2021, volume=59, issue=1, pageStart=183, pageEnd=191, url=null, language=null, rfNumber=［30］, rfOrder=29, authorNames=ZHENG J, HU S, WANG J, journalName=Pharm Biol, refType=null, unstructuredReference=ZHENG J，HU S，WANG J，et al. Icariin improves brain function decline in aging rats by enhancing neuronal autophagy through the AMPK/mTOR/ULK1 pathway［J］. 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注：A.正常组；B.模型组；C.艾司西酞普兰组；D.柴胡疏肝散低剂量组；E.柴胡疏肝散中剂量组；F.柴胡疏肝散高剂量组。

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注：A.正常组；B.模型组；C.艾司西酞普兰组；D.柴胡疏肝散低剂量组；E.柴胡疏肝散中剂量组；F.柴胡疏肝散高剂量组。

, figureFileSmall=+SYECxPc4P5g2FcT+I6nhA==, figureFileBig=Z2DLcSoOpveTI6q8LbyswQ==, tableContent=null), ArticleFig(id=1322926928910492155, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=7fAdDTAKDi2c+GlDA41BVQ==, figureFileBig=bv0snbwXUrjPOs88RolzPg==, tableContent=null), ArticleFig(id=1322926928981795324, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=图3, caption=各组大鼠OFC组织中胶质纤维酸性蛋白（GFAP）表达（×200）

注：A.正常组；B.模型组；C.艾司西酞普兰组；D.柴胡疏肝散低剂量组；E.柴胡疏肝散中剂量组；F.柴胡疏肝散高剂量组。

, figureFileSmall=7fAdDTAKDi2c+GlDA41BVQ==, figureFileBig=bv0snbwXUrjPOs88RolzPg==, tableContent=null), ArticleFig(id=1322926929053098493, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=Gc4UtlTDN+Ry9aVSeziVLQ==, figureFileBig=uiqkFkXuFFYFGmEHdc42tw==, tableContent=null), ArticleFig(id=1322926929170539006, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=图4, caption=各组大鼠OFC组织中pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的蛋白印迹图

注：1：正常组；2：模型组；3：艾司西酞普兰组；4：柴胡疏肝散低剂量组；5：柴胡疏肝散中剂量组；6：柴胡疏肝散高剂量组。

, figureFileSmall=Gc4UtlTDN+Ry9aVSeziVLQ==, figureFileBig=uiqkFkXuFFYFGmEHdc42tw==, tableContent=null), ArticleFig(id=1322926929246036479, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
基因引物长度/（bp）
AMPKForward：5′-AGTGTGTGAGAAGTTCGAGTGCT-3′108
Reverse：5′-CTGTTGTCTATTATGAGGTGGTAGG-3′
ULK1Forward：5＇-CACTGACAGCCTACAGGAGAAAC-3＇190
Reverse：5＇-GGAAGAGCCCACTGAGAACAT-3＇
mTORForward：5＇-TGCTGAGTATGTGGAGTTTGAAGT-3＇132
Reverse：5＇-TGGAAGAAGAAGGTGGGGAC-3＇
β-actinForward：5＇-CCTAGACTTCGAGCAAGAGA-3＇140
Reverse：5＇-GGAAGGAAGGCTGGAAGA-3＇
), ArticleFig(id=1322926929355088384, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=表1, caption=

AMPK、ULK1、mTOR引物序列

, figureFileSmall=null, figureFileBig=null, tableContent=
基因引物长度/（bp）
AMPKForward：5′-AGTGTGTGAGAAGTTCGAGTGCT-3′108
Reverse：5′-CTGTTGTCTATTATGAGGTGGTAGG-3′
ULK1Forward：5＇-CACTGACAGCCTACAGGAGAAAC-3＇190
Reverse：5＇-GGAAGAGCCCACTGAGAACAT-3＇
mTORForward：5＇-TGCTGAGTATGTGGAGTTTGAAGT-3＇132
Reverse：5＇-TGGAAGAAGAAGGTGGGGAC-3＇
β-actinForward：5＇-CCTAGACTTCGAGCAAGAGA-3＇140
Reverse：5＇-GGAAGGAAGGCTGGAAGA-3＇
), ArticleFig(id=1322926929443168769, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量糖水偏好系数悬浮不动时间/（s）旷场行走路程/（cm）
正常组100.79±0.08 68.57±5.57 3 196.20±167.68
模型组100.34±0.10**115.38±8.51**2 488.42±114.25**
艾司西酞普兰组1010.50 mg/kg0.66±0.06**##75.90±7.60##3 053.08±143.33##
柴胡疏肝散低剂量组103.15 g/kg0.62±0.05**##79.16±5.83**##2 860.13±125.42**##
柴胡疏肝散中剂量组106.30 g/kg0.59±0.06**##77.59±7.51**##2 805.48±295.01**##
柴胡疏肝散高剂量组1012.60 g/kg0.66±0.06**##72.39±6.43##3 063.51±314.53##○○
F值44.37559.43414.446
P值P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929548026370, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=表2, caption=

各组大鼠行为学检测结果比较（）

, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量糖水偏好系数悬浮不动时间/（s）旷场行走路程/（cm）
正常组100.79±0.08 68.57±5.57 3 196.20±167.68
模型组100.34±0.10**115.38±8.51**2 488.42±114.25**
艾司西酞普兰组1010.50 mg/kg0.66±0.06**##75.90±7.60##3 053.08±143.33##
柴胡疏肝散低剂量组103.15 g/kg0.62±0.05**##79.16±5.83**##2 860.13±125.42**##
柴胡疏肝散中剂量组106.30 g/kg0.59±0.06**##77.59±7.51**##2 805.48±295.01**##
柴胡疏肝散高剂量组1012.60 g/kg0.66±0.06**##72.39±6.43##3 063.51±314.53##○○
F值44.37559.43414.446
P值P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929623523843, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量Iba-1MBPGFAP
正常组105.37±1.2725.87±1.959.42±0.90
模型组1012.30±1.88**15.32±2.02**23.51±1.48**
艾司西酞普兰组1010.50 mg/kg6.65±1.11*##19.68±2.02**##11.01±0.91**##
柴胡疏肝散低剂量组103.15 g/kg7.78±0.98##**21.63±1.96**##△11.69±1.25**##
柴胡疏肝散中剂量组106.30 g/kg7.46±1.53##19.94±2.15**##11.32±1.03**##
柴胡疏肝散高剂量组1012.60 g/kg5.96±1.37##▲▲○20.67±1.33**##10.15±0.97##▲▲○
F值31.83331.402226.533
P值P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929711604228, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=表3, caption=

各组大鼠OFC组织中Iba-1、MBP、GFAP平均光密度比较（）

, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量Iba-1MBPGFAP
正常组105.37±1.2725.87±1.959.42±0.90
模型组1012.30±1.88**15.32±2.02**23.51±1.48**
艾司西酞普兰组1010.50 mg/kg6.65±1.11*##19.68±2.02**##11.01±0.91**##
柴胡疏肝散低剂量组103.15 g/kg7.78±0.98##**21.63±1.96**##△11.69±1.25**##
柴胡疏肝散中剂量组106.30 g/kg7.46±1.53##19.94±2.15**##11.32±1.03**##
柴胡疏肝散高剂量组1012.60 g/kg5.96±1.37##▲▲○20.67±1.33**##10.15±0.97##▲▲○
F值31.83331.402226.533
P值P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929812267525, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量pT172-AMPKAMPKpS2448-mTORmTORpS757-ULK1ULK1
正常组100.69±0.04 0.82±0.12 0.87±0.08 0.86±0.14 0.75±0.04 0.76±0.06
模型组100.35±0.09**0.55±0.06**0.48±0.08**0.63±0.06**0.47±0.09**0.49±0.08**
艾司西酞普兰组1010.50 mg/kg0.61±0.07*##0.79±0.04##0.68±0.15**0.83±0.11##0.61±0.08**##0.67±0.07*##
柴胡疏肝散低剂量组103.15 g/kg0.59±0.11**##0.71±0.07△**##0.65±0.12**##0.74±0.07**#0.65±0.07**##0.65±0.07**##
柴胡疏肝散中剂量组106.30 g/kg0.62±0.08*##0.74±0.08*##0.61±0.08**#0.75±0.09*##0.66±0.08##0.66±0.10**##
柴胡疏肝散高剂量组1012.60 g/kg0.62±0.08*##0.81±0.08##▲▲0.72±0.14**##○0.82±0.08##0.70±0.12##△0.72±0.09##▲
F值21.65816.81813.5467.17313.89614.253
P值P<0.001P<0.001P<0.001P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929883570694, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=表4, caption=

各组大鼠OFC组织中pT172-AM PK/AM PK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1蛋白表达（）

, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量pT172-AMPKAMPKpS2448-mTORmTORpS757-ULK1ULK1
正常组100.69±0.04 0.82±0.12 0.87±0.08 0.86±0.14 0.75±0.04 0.76±0.06
模型组100.35±0.09**0.55±0.06**0.48±0.08**0.63±0.06**0.47±0.09**0.49±0.08**
艾司西酞普兰组1010.50 mg/kg0.61±0.07*##0.79±0.04##0.68±0.15**0.83±0.11##0.61±0.08**##0.67±0.07*##
柴胡疏肝散低剂量组103.15 g/kg0.59±0.11**##0.71±0.07△**##0.65±0.12**##0.74±0.07**#0.65±0.07**##0.65±0.07**##
柴胡疏肝散中剂量组106.30 g/kg0.62±0.08*##0.74±0.08*##0.61±0.08**#0.75±0.09*##0.66±0.08##0.66±0.10**##
柴胡疏肝散高剂量组1012.60 g/kg0.62±0.08*##0.81±0.08##▲▲0.72±0.14**##○0.82±0.08##0.70±0.12##△0.72±0.09##▲
F值21.65816.81813.5467.17313.89614.253
P值P<0.001P<0.001P<0.001P<0.001P<0.001P <0.001
), ArticleFig(id=1322926929963262471, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量AMPK mRNAmTOR mRNAULK1 mRNA
正常组102.06±0.111.35±0.141.34±0.32
模型组100.89±0.14**0.62±0.13**0.72±0.17**
艾司西酞普兰组1010.50 mg/kg1.68±0.15##1.20±0.18**##1.14±0.19*##
柴胡疏肝散低剂量组103.15 g/kg1.68±0.14**##1.05±0.19**##1.03±0.14**##
柴胡疏肝散中剂量组106.30 g/kg1.69±0.13##1.00±0.19**##△0.99±0.08**##
柴胡疏肝散高剂量组1012.60 g/kg1.82±0.13##△▲○1.16±0.35*##1.34±0.23##△▲▲○○
F值87.48113.88313.582
P值P<0.001P<0.001P <0.001
), ArticleFig(id=1322926930055537160, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926921641763270, language=CN, label=表5, caption=

各组大鼠OFC组织中AMPK、mTOR、ULK1 mRNA的表达（）

, figureFileSmall=null, figureFileBig=null, tableContent=
组别n剂量AMPK mRNAmTOR mRNAULK1 mRNA
正常组102.06±0.111.35±0.141.34±0.32
模型组100.89±0.14**0.62±0.13**0.72±0.17**
艾司西酞普兰组1010.50 mg/kg1.68±0.15##1.20±0.18**##1.14±0.19*##
柴胡疏肝散低剂量组103.15 g/kg1.68±0.14**##1.05±0.19**##1.03±0.14**##
柴胡疏肝散中剂量组106.30 g/kg1.69±0.13##1.00±0.19**##△0.99±0.08**##
柴胡疏肝散高剂量组1012.60 g/kg1.82±0.13##△▲○1.16±0.35*##1.34±0.23##△▲▲○○
F值87.48113.88313.582
P值P<0.001P<0.001P <0.001
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柴胡疏肝散对抑郁症模型大鼠AMPK/mTOR/ULK1通路及胶质细胞的作用
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程茗 , 曹峰 , 张震
中华中医药学刊 | 国家项目点击 2025,43(10): 176-181
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中华中医药学刊 |国家项目点击 2025 , 43 (10) : 176 -181
柴胡疏肝散对抑郁症模型大鼠AMPK/mTOR/ULK1通路及胶质细胞的作用
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程茗, 曹峰, 张震
作者信息
  • 贵州中医药大学，贵州 贵阳 550025
通讯作者:
张震（1987-），男，山东潍坊人，副教授，硕士研究生导师，博士，博士后，研究方向：中医肝藏象情志致病。E-mail：。
作者简介:

程茗（1999-），女，山东烟台人，硕士在读，研究方向：中医情志病防治。

Effects of Chaihu Shugan Powder（柴胡疏肝散）on AMPK/mTOR/ULK1 Pathway and Glial Gells in Depression Model Rats
Ming CHENG, Feng CAO, Zhen ZHANG
Affiliations
  • Guizhou University of Traditional Chinese Medicine，Guiyang550025，Guizhou，China
出版时间: 2025-10-10 doi: 10.13193/j.issn.1673-7717.2025.10.033
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摘要
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目的

探讨柴胡疏肝散对抑郁症模型大鼠眶额皮层（OFC）腺苷酸活化蛋白激活酶（AMPK）/哺乳动物雷帕霉素靶蛋白（mTOR）/UNC-51样激酶1（ULK1）通路及胶质细胞的调控作用。

方法

采用慢性不可预测轻度应激（CUMS）法制备抑郁症大鼠模型。按照随机数字表法选取10只大鼠作为正常组，将造模成功的50只大鼠按随机数字表法分为模型组、艾司西酞普兰组（10.50 mg/kg）、柴胡疏肝散低剂量组（3.15 g/kg）、柴胡疏肝散中剂量组（6.30 g/kg）、柴胡疏肝散高剂量组（12.60 g/kg），每组10只，连续灌胃28 d。观察各组大鼠糖水偏好系数、悬浮不动时间、旷场行走路程的变化。待上述检测完成后断头取脑，采用免疫荧光法检测大鼠OFC中离子钙结合受体分子1（Iba-1）、髓鞘碱性蛋白（MBP）、胶质纤维酸性蛋白（GFAP）的表达；Western blotting法检测OFC中pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的蛋白表达；实时荧光PCR法检测OFC中AMPK、mTOR、ULK1 mRNA的表达。

结果

与正常组比较，模型组及各给药组糖水偏好系数降低、悬浮不动时间增加、旷场行走路程减少（P<0.05，P<0.01）；与模型组比较，各给药组的糖水偏好系数升高、悬浮不动时间减少、旷场行走路程均有所升高（P<0.01）；与正常组比较，Iba-1及GFAP除柴胡疏肝散高剂量组外，模型组及各给药组Iba-1及GFAP均升高（P<0.05，P<0.01），MBP均降低（P<0.01）；与模型组比较，各给药组Iba-1、GFAP均降低（P<0.01）、MBP均升高（P<0.01）；与正常组比较，模型组及各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR及pS757-ULK1/ULK1蛋白表达均降低（P<0.05，P<0.01）；与模型组比较，各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR、pS757-ULK1/ULK1蛋白表达均升高（P<0.05）；与正常组比较，模型组、艾司西酞普兰组及柴胡疏肝散低、中剂量组mTOR、ULK1 mRNA表达均降低（P<0.01），柴胡疏肝散低剂量组的AMPK mRNA、柴胡疏肝散低、高剂量组的mTOR mRNA表达降低（P<0.05，P<0.01）；与模型组比较，各给药组AMPK mRNA、mTOR mRNA、ULK1 mRNA表达均升高（P<0.01）。

结论

柴胡疏肝散可以通过降低大鼠OFC组织中Iba-1、GFAP，升高MBP的表达，激活AMPK/mTOR/ULK1通路以发挥其抗抑郁作用。

柴胡疏肝散  /  抑郁症  /  慢性不可预测轻度应激  /  眶额皮层  /  胶质细胞
Objective

To investigate the regulatory effects of Chaihu Shugan Powder（柴胡疏肝散）on the adenylate-activated protein activating enzyme（AMPK）/mammalian target of rapamycin（mTOR）/UNC-51-like kinase 1（ULK1）pathway and glial cells in the orbitofrontal cortex（OFC）of depression model rats.

Methods

The rat model of depression was established by chronic unpredictable mild stress（CUMS）.According to the random number table，10 rats were selected as the normal group and 50 rats with successful modeling were divided into model group，escitalopram group（10.50 mg/kg），Chaihu Shugan Powder lowdose group（3.15 g/kg），Chaihu Shugan Powder middle-dose group（6.30 g/kg），Chaihu Shugan Powder high-dose group（12.60 g/kg）according to the random number table，with ten rats in each group for 28 consecutive days.The changes of sugar preference coefficient，suspension immobility time and open field walking distance of rats in each group were observed.After the above detection was completed，the head was decapitated and the brain was removed，and the expressions of ionized calciumbinding receptor molecule 1（Iba-1），myelin basic protein（MBP）and glial fibrillary acidic protein（GFAP）in rat OFC tissues were detected by immunofluorescence assay.Western blotting method was used to detect the protein expressions of pT172-AMPK/AMPK，pS2488-mTOR/mTOR and pS757-ULK1/ULK1 in OFC tissue.The expressions of AMPK，mTOR and ULK1 mRNA in OFC were detected by real-time PCR.

Results

Compared to the control group，the model group and each treatment group showed a decrease in sucrose preference coefficient，an increase in immobility time in the forced swimming test and a decrease in distance traveled in the open field test（P<0.05，P<0.01）.Compared to the model group，each treatment group showed an increase in sucrose preference coefficient，a decrease in immobility time and an increase in distance traveled in the open field test（P<0.01）.Compared to the control group，the model group and each treatment group showed an increase in protein expressions of Iba-1 and GFAP（P<0.05，P<0.01），and a decrease in MBP protein expression（P<0.01），except those in the Chaihu Shugan Powder low-dose group.Compared to the model group，each treatment group showed a decrease in protein expressions of Iba-1 and GFAP（P<0.01），and an increase in MBP protein expression（P<0.01）.Compared to the control group，the model group and each treatment group showed a decrease in protein expressions of pT172-AMPK/AMPK，pS2448-mTOR/mTOR and pS757-ULK1/ULK1（P<0.05，P<0.01）.Compared to the model group，each treatment group showed an increase in protein expressions of pT172-AMPK/AMPK，pS2448-mTOR/mTOR and pS757-ULK1/ULK1（P<0.05）.Compared to the control group，the model group，escitalopram group，Chaihu Shugan Powder low-dose group and middle-dose group showed a decrease in expressions of mTOR and ULK1 mRNA（P<0.01），Chaihu Shugan Powder low-dose group showed a decrease in AMPK mRNA expression（P<0.05），and the Chaihu Shugan Powder high-dose group group showed a decrease in mTOR mRNA expression（P<0.01）.Compared to the model group，each treatment group showed an increase in expressions of AMPK mRNA，mTOR mRNA nd ULK1 mRNA（P<0.01）.

Conclusion

Chaihu Shugan Powder can reduce the expressions of Iba-1 and GFAP in OFC of rats，increase the expression of MBPand activate AMPK/mTOR/ULK1 pathway expression to exert the antidepressant effect.

Chaihu Shugan Powder（柴胡疏肝散）  /  depression  /  chronic unpredictable mild stress  /  orbitofrontal cortex  /  glial cells
程茗, 曹峰, 张震. 柴胡疏肝散对抑郁症模型大鼠AMPK/mTOR/ULK1通路及胶质细胞的作用. 中华中医药学刊, 2025 , 43 (10) : 176 -181 . DOI: 10.13193/j.issn.1673-7717.2025.10.033
Ming CHENG, Feng CAO, Zhen ZHANG. Effects of Chaihu Shugan Powder（柴胡疏肝散）on AMPK/mTOR/ULK1 Pathway and Glial Gells in Depression Model Rats[J]. Chinese Archives of Traditional Chinese Medicine, 2025 , 43 (10) : 176 -181 . DOI: 10.13193/j.issn.1673-7717.2025.10.033
正文
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抑郁症是以持续的心境低落为主要临床特征的心理疾病，严重者亦伴有明显的自杀倾向[1]。抑郁症病因病机复杂，发病机制尚未明确，因此探索抑郁症的发病机制及寻求新的靶向药物对临床治疗该病具有重要意义。本团队前期研究发现，采用慢性不可预测轻度应激（CUMS）法制备的抑郁症模型大鼠眶额皮层（OFC）脑区小胶质细胞的表达异常[2]，而未见少突胶质细胞、星形胶质细胞是否参与其调控的相关报道。有研究表明腺苷酸活化蛋白激活酶（AMPK）/哺乳动物雷帕霉素靶蛋白（mTOR）/UNC-51样激酶1（ULK1）通路在自噬调控中发挥重要作用[3-5]，但未见该通路在抑郁症中的相关研究。柴胡疏肝散出自《景岳全书》，为疏肝解郁的代表方剂，目前大量研究已经证实柴胡疏肝散有较好的抗抑郁作用[6-7]。本研究基于前期研究，将柴胡疏肝散作为干预方剂，观察抑郁症模型大鼠OFC中小胶质细胞、少突胶质细胞及星形胶质细胞及AMPK/mTOR/ULK1通路的变化，以期为抑郁症的临床诊疗提供更多的科学依据。
1　材料
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1.1　动物
健康SD大鼠85只，雄性，SPF级，6～8周龄，体质量200～220 g，购自湖北省实验动物研究中心，生产许可证号：SCXK（鄂）2015-0018。所有大鼠饲养于贵州中医药大学中医药实验中心，温度20～25℃，湿度50%～65%，12 h交替照明，自由饮食、摄水。
1.2　伦理审查
本研究经贵州中医药大学实验动物伦理审查委员会批准通过，批件编号：20220004。
1.3　药物
柴胡疏肝散药用：柴胡168 g，陈皮168 g，川芎140 g，香附140 g，枳壳140 g，白芍140 g，炙甘草84 g。方中所有药材饮片均购自北京同仁堂药店，将所有中药浸泡30 min后，加水1 500 mL煎煮30 min，收集药液，药渣加入等量水后重复煎煮1次，将2次煎煮后的药液合并，浓缩至含生药量1.26 g/mL作为柴胡疏肝散高剂量组药液，依次加入蒸馏水稀释，配制柴胡疏肝散中剂量组（0.63 g/mL）药液和低剂量组（0.315 g/mL）药液。草酸艾司西酞普兰片（规格10 mg/片，国药准字H20080788，批号：S14202181829，四川科伦药业股份有限公司），将草酸艾司西酞普兰片碾压成粉末，加入生理盐水配置成0.3 g/L的溶液。
1.4　主要试剂及仪器
兔抗AMPK、兔抗mTOR、兔抗ULK1、QuickBlock Western一抗和二抗稀释液、QuickBlock TM免疫染色二抗稀释液（中国碧云天生物技术有限公司，批号：AF1627、AF1648、AF8307、P0239、P0258），胶质纤维酸性蛋白（GFAP）抗体（美国BioVision公司，批号：3206-200），离子钙结合受体分子1（Iba-1）抗体（英国Abcam公司，批号：ab178846），髓鞘碱性蛋白（MBP）抗体（爱必信上海生物科技有限公司，批号：abs106147），BCA蛋白质定量试剂盒（北京普利莱基因技术有限公司，批号：P1511-1），逆转录试剂盒［宝日医生物技术（北京）有限公司，批号：RR047A］，染料法荧光定量试剂盒［宝日医生物技术（北京）有限公司，批号：RR820A］
Leica TCS SP5激光共聚焦显微镜（德国Leica公司），DYY-7C型电泳仪、DYCZ-40型电转仪（北京六一仪器厂），BioPhotometer D30核酸蛋白测定仪（德国艾本德公司），LDZ5-2低速离心机（北京京立离心机有限公司），H-7500型透射电子显微镜（日本日立公司），ABI7500型荧光定量PCR仪（美国ABI公司）。
2　方法
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2.1　造模及分组
将85只大鼠按照随机数字表法分为正常组10只和造模组75只。参考文献［8］，将造模组75只大鼠采用CUMS法制备抑郁症大鼠模型。分笼饲养，并每日随机接受1种应激刺激，如断水24 h、断食24 h、夹尾1 min、4℃冰水游泳5 min、摇晃（1次/s，持续5 min）、昼夜颠倒、电击足底（电压50 mV，每5 s刺激1次，间歇5 s，共刺激10次），相邻2 d不能接受同种刺激，每种刺激平均使用4次。连续28 d后，糖水消系数、悬浮不动时间及旷场行走路程较应激刺激实验开始前存在明显差异（P<0.05），视为造模成功[7，9]。将造模成功的50只大鼠按照随机数字表法分为模型组，艾司西酞普兰组，柴胡疏肝散低、中、高剂量组，每组10只。
2.2　给药
按照人和动物体表面积折算的等效剂量比率表换算高、中、低剂量分别为12.60、6.30、3.15 g/kg，参考文献［10］确定艾司西酞普兰的给药剂量为10.50 mg/kg，按3.15 mL/kg灌胃，正常组与模型组大鼠灌胃等体积的生理盐水，各组每日灌胃1次，连续28 d。
2.3　样本采集
各组大鼠行为学检测后，使用1%戊巴比妥纳腹腔注射麻醉，断头取脑。冰上剥离大鼠OFC组织，液氮冻存24 h后置于-80℃冰箱保存。
2.4　指标检测
2.4.1　行为学检测
（1）糖水偏好实验：通过观察大鼠蔗糖水消耗情况探索其抑郁状态，蔗糖水消耗量越大说明抑郁状态越轻。给药结束后进行糖水偏好训练，每只大鼠（单笼饲养）饲养笼上放置2个水瓶，训练第1天给予2瓶1%蔗糖溶液，第2天将其中1瓶1%蔗糖水溶液换为日常饮用水。2 d训练结束后，所有大鼠禁食禁水24 h后，正式进行糖水偏好实验。实验前测定糖水偏好基线，实验期间大鼠自由选择饮用1%蔗糖水溶液或日常饮用水，第28天进行糖水偏好系数测定。糖水偏好系数＝蔗糖水消耗量/（蔗糖水消耗量+日常饮用水消耗量）。
（2）强迫游泳实验：通过观察大鼠悬浮不动时间探索其抑郁状态，悬浮不动时间越长说明抑郁状态越严重。强迫游泳实验装置为高50 cm、直径20 cm的圆柱形有机玻璃容器，水温（25±1）℃，水深30 cm。给药结束后，每只大鼠接受15 min的强迫游泳训练，并在第2天进行强迫游泳实验。每只大鼠进行强迫游泳实验6 min，在最后4 min记录不动时间。大鼠保持头部悬浮在水面上并且无明显挣扎的时间为悬浮不动时间。
（3）旷场实验：使用旷场实验检测大鼠的自发运动能力、探索能力和焦虑情绪，路程越长说明自发运动能力、探索能力越强和焦虑情绪越轻。给药结束后，将待测大鼠放在规格为50 cm×50 cm×50 cm的旷场箱底板中心5 min，记录小鼠在整个旷场的行走路程（cm）。每只大鼠实验完成后，用75%乙醇擦拭旷场箱底面，去除气味减少对下一只大鼠的干扰。
2.4.2　免疫荧光法检测大鼠OFC组织中Iba-1、MBP、GFAP的表达
将OFC脑组织放入4℃0.9%NaCl溶液中预冷，4%多聚甲醛灌流固定，石蜡包埋后制成5μm组织切片，将切片放置于24孔板中，使用PBS缓冲液冲洗3次，每次10 min，摇床处理。将清洗后的切片放置于免疫荧光封闭液中，室温下进行孵育1 h。4℃下加入Iba-1、MBP、GFAP一抗孵育过夜，PBS清洗3次，每次10 min，摇床，室温。加入Iba-1、MBP、GFAP二抗孵育后，PBS清洗3次，每次10 min。染色后的切片置于载玻片上，滴加DAPI封片液后，显微镜下拍照，采用Image Pro Plus 6.0，单张图片校正后选定测量项目及范围，测量后输出照片数据，统一参数条件下测定图像平均光密度值。
2.4.3　Western blotting法检测OFC组织中pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的蛋白表达
取大鼠OFC组织50 mg，加入蛋白裂解液，冰上研磨，4℃12 000 r/min，半径15 cm，离心30 min。取上层清液，使用BCA蛋白定量试剂盒对各组蛋白量分别测定，依次进行加样、电泳以及转膜等处理，按照说明书要求操作，采用凝胶图像成像分析系统测定蛋白表达量，蛋白表达量以目的蛋白的灰度值与β-actin的灰度值的比值表示。
2.4.4　实时荧光PCR检测OFC组织中AMPK、mTOR、ULK1 mRNA表达
取OFC组织100 mg，采用Trizol法提取总mRNA，按照Takara逆转录试剂盒说明书逆转录合成cDNA，按照SYBR Premix Ex TaqII染料法荧光定量试剂盒说明书进行操作，荧光定量PCR仪进行基因扩增。以β-actin为内参，数据采用RQ＝2-△△Ct法计算相对表达量。引物序列见表1，引物序列由武汉谷歌生物科技公司合成。
2.5　统计学方法
本研究采用SPSS 26.0软件进行数据处理，符合正态分布的计量资料以均值±标准差（）表示。方差齐则多组间比较采用单因素方差分析，组间两两比较采用LSD检验，方差不齐采用Welch＇sANOVA分析，两两比较采用Dunnett＇s T3检验，以P<0.05为差异有统计学意义。
3　结果
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3.1　各组大鼠行为学检测
与正常组比较，模型组及各给药组糖水偏好系数降低、悬浮不动时间增加、旷场行走路程减少（P<0.05，P<0.01）；与模型组比较，各给药组的糖水偏好系数升高、悬浮不动时间减少、旷场行走路程均有所升高（P<0.01）。结果见表2。
3.2　免疫荧光法检测OFC组织Iba-1、MBP、GFAP的表达
与正常组比较，Iba-1及GFAP除柴胡疏肝散高剂量组外，模型组及各给药组Iba-1及GFAP均升高（P<0.05，P<0.01），MBP均降低（P<0.01）；与模型组比较，各给药组Iba-1、GFAP均降低（P<0.01）、MBP均升高（P<0.01）。结果见插页ⅩⅩⅤ图1、插页ⅩⅩⅥ图2、插页ⅩⅩⅦ图3、表3。
3.3　Western boltting法检测OFC组织pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的表达
与正常组比较，模型组及各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR及pS757-ULK1/ULK1蛋白表达均降低（P<0.05，P<0.01）；与模型组比较，各给药组pT172-AMPK/AMPK、pS2448-mTOR/mTOR、pS757-ULK1/ULK1蛋白表达均升高（P<0.05）。结果见图4、表4。
3.4　各组大鼠OFC组织中AMPK、mTOR、ULK1 mRNA表达结果
与正常组比较，模型组、艾司西酞普兰组及柴胡疏肝散低、中剂量组mTOR、ULK1 mRNA表达均降低（P<0.01），柴胡疏肝散低剂量组的AMPK mRNA、柴胡疏肝散低、高剂量组的mTORmRNA表达降低（P<0.05，P<0.01）；与模型组比较，各给药组AMPKmRNA、mTORmRNA、ULK1 mRNA表达均升高（P<0.01）。结果见表5。
4　讨论
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中医学中并无抑郁症之说，根据抑郁症临床表现可归属于“百合病”“郁病”“脏躁”等范畴[11]。《素问·脉要精微论篇》中记载“头者，精明之府”，是对脑主神明的最早论述，《颅囟经》中有记载“元神在头曰泥丸，总众神也”，意在说明神是人体五志的统属，而神藏于脑中，也明确了五志由脑统属[12]。张景岳《类经》注道：“人之脑为髓海，是谓上丹田，太乙帝君所居。”亦称太乙帝君，即泥丸君，又称太乙元真，为至尊无上之元神和脑神。脑为奇恒之腑，主神志思维活动，大脑在精神、神志疾病中发挥着非常重要的作用[13]。肝主疏泄，主藏血，肝疏泄正常，则气血和调，上荣于脑，则脑清神聪；若疏泄失常，气血逆乱，脑失所养，则脑主宰精神活动失常，钱镜湖在《辨证奇闻》中亦提出“脑气不足治在肝”的观点。柴胡疏肝散源于张介宾《景岳全书》，该方是在四逆汤的基础上加陈皮、川芎、香附以增强疏肝行气之效，后世将其作为治疗肝气郁滞的常用方剂，现代药理研究证实柴胡疏肝散具有抗抑郁的作用。
本团队前期针对抑郁症OFC的研究发现抑郁症模型大鼠OFC组织表面粗糙，细胞肿胀明显，神经嗜染质减少，且OFC组织中BDNF、TrkB、p-ERK蛋白及mRNA表达水平均呈现异常，说明OFC参与了抑郁症的发病过程。一项关于首发抑郁障碍患者经草酸艾司西酞普兰治疗8周的研究发现[14]，患者内侧OFC脑区局部皮层折叠系数降低。AFRIDI R等[15]研究发现抑郁症患者双侧眶额和左侧颞中回灰质体积较健康者减小。LI C等[16]研究发现难治性抑郁症患者的OFC的静息态脑功能磁共振ReHo值与冗思量表评分呈正相关。OFC属于情绪调控的关键脑区，抑郁症患者出现OFC过度激活时，会对社会拒绝信号表现出高强反应，增加抑郁症患者的自杀风险。
本团队前期研究发现，抑郁症模型组大鼠小胶质细胞的表达存在异常。有研究发现[17-19]，抑郁症大鼠杏仁核内产生的炎症因子激活小胶质细胞，产生补体成分，激活的小胶质细胞诱导星形胶质细胞变为具有神经毒性星形胶质细胞而诱发抑郁样行为。杨皓然等[20]研究发现逍遥散可抑制海马M1型小胶质细胞极化，减轻中枢炎性反应而产生抗抑郁作用。ZONG J等[21]研究发现罗格列酮能够增加CMS小鼠前额叶皮层中星形胶质细胞的数量，并改善神经元轴突的密度。我们在前期研究发现小胶质细胞标志物Iba-1在模型组大鼠OFC组织中表达异常。本研究在前期研究基础上，观察星形胶质细胞、少突胶质细胞是否也均参与抑郁症的发病。结果发现，模型组大鼠OFC组织中小胶质细胞标志物Iba-1、星形胶质细胞标志物GFAP表达升高，少突胶质细胞标志物MBP表达降低，表明除小胶质细胞外，星形胶质细胞和少突胶质细胞也与抑郁症的发病相关。
AMPK在自噬调控方面发挥着能量调控的重要作用[22-24]。AMPK一方面可通过抑制mTOR蛋白复合体1活化来促进自噬；另一方面自噬启动因子ULK1复合体可以在AMPK作用下磷酸化S317、S467、S555、T575、S637和S777等多个位点促进自噬[25-27]。当AMPK活性受到抑制时，mTORC1活化能力增强，而mTORC1对ULK1丝氨酸757位点的磷酸化起到促进作用，进而使自噬受抑制[28-30]。本次研究我们采用Western blotting法检测OFC组织中AMPK、mTOR、ULK1及其磷酸化蛋白的表达水平，观察AMPK/mTOR/ULK1信号通路的变化。结果显示，与正常组比较，模型组pT172-AMPK/AMPK、pS2448-mTOR/mTOR、pS757-ULK1/ULK1均表达异常，且药物干预后柴胡疏肝散高剂量组大鼠OFC组织中pT172-AMPK/AMPK、pS2488-mTOR/mTOR、pS757-ULK1/ULK1的蛋白表达水平升高；实时荧光PCR法检测结果显示，柴胡疏肝散高剂量组较模型组大鼠的AMPK、mTOR、ULK1 mRNA表达均存在差异。
综上所述，抑郁症的发病机制可能与Iba-1及GFAP表达水平升高、MBP表达水平降低、AMPK、mTOR、ULK1蛋白及mRNA表达水平降低有关。本研究虽然对小胶质细胞、星形胶质细胞、少突胶质细胞的表达情况进行了研究，但这3种胶质细胞是否呈现差异性，本次研究未做相关统计。抑郁症大鼠胶质细胞胞内AMPK/mTOR/ULK1自噬通路的变化是否与胶质细胞的表达存在相关性，本文也未做深入研究。后期可体外培养胶质细胞，借助AMPK/mTOR/ULK1通路的抑制剂或激动剂，进一步研究胶质细胞中AMPK/mTOR/ULK1自噬通路的表达情况，为AMPK/mTOR/ULK1自噬通路与胶质细胞的关系提供依据。
基金
收起
  • 国家自然科学基金项目(82160863; 82160920)
  • 中国博士后科学基金项目(2022M711733)
  • 贵州省自然科学基金项目(黔科合基础-ZK〔2022〕一般511)
  • 河北省博士后择优资助项目(B2022003040)
  • 贵州省卫生健康委员会科学技术基金项目(gzwkj2023-148)
  • 贵州省中医药、民族医药科学技术研究项目(QZYY-2024-011)
  • 贵州中医药大学研究生教育创新计划项目(YCXKYS2023027)
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2025年第43卷第10期
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doi: 10.13193/j.issn.1673-7717.2025.10.033
  • 首发时间：2026-10-30
  • 出版时间：2025-10-10
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基金
国家自然科学基金项目(82160863; 82160920)
中国博士后科学基金项目(2022M711733)
贵州省自然科学基金项目(黔科合基础-ZK〔2022〕一般511)
河北省博士后择优资助项目(B2022003040)
贵州省卫生健康委员会科学技术基金项目(gzwkj2023-148)
贵州省中医药、民族医药科学技术研究项目(QZYY-2024-011)
贵州中医药大学研究生教育创新计划项目(YCXKYS2023027)
作者信息
    贵州中医药大学，贵州 贵阳 550025

通讯作者:

张震（1987-），男，山东潍坊人，副教授，硕士研究生导师，博士，博士后，研究方向：中医肝藏象情志致病。E-mail：。
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Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
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Number of
species		 占总种数比例
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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