Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway
Wuzi Yanzong Pill (WYP) was found to play a protective role on nerve cells and neurological diseases, however the molecular mechanism is unclear. To understand the molecular mechanisms that underly the neuroprotective effect of WYP on dopaminergic neurons in Parkinson’s disease (PD). PD mouse model...
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| Veröffentlicht in: | Metabolic brain disease 2022-06, Vol.37 (5), p.1435-1450 |
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| creator | Hang, Wei Fan, Hui-jie Li, Yan-rong Xiao, Qi Jia, Lu Song, Li-juan Gao, Yao Jin, Xiao-ming Xiao, Bao-guo Yu, Jie-zhong Ma, Cun-gen Chai, Zhi |
| description | Wuzi Yanzong Pill (WYP) was found to play a protective role on nerve cells and neurological diseases, however the molecular mechanism is unclear. To understand the molecular mechanisms that underly the neuroprotective effect of WYP on dopaminergic neurons in Parkinson’s disease (PD). PD mouse model was induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Gait and hanging tests were used to assess motor behavioral function. Immunofluorescence assay was used to determine TH-positive neurons in substantia nigra (SN). Apoptosis, dopamine and neurotrophic factors as well as expression of PI3K/Akt pathway were detected by TUNEL staining, ELISA and western blotting, respectively. First, it was observed that WYP intervention improved abnormal motor function in MPTP-induced PD model, alleviated the loss of TH
+
neurons in SN, and increased dopamine content in brain, revealing a potential protective effect. Second, network pharmacology was used to analyze the possible targets and pathways of WYP action in the treatment of PD. A total of 126 active components related to PD were screened in WYP, and the related core targets included ALB, GAPDH, Akt1, TP53, IL6 and TNF. Particularly, the effect of WYP on PD may be medicate through PI3K/Akt signaling pathway and apoptotic regulation. The WYP treated PD mice had higher expression of p-PI3K, p-Akt and Bcl-2 but lower expression of Bax and cleaved caspase-3 than the non-WYP treated PD mice. Secretion of brain-derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) were also increased in the treated mice. WYP may inhibit apoptosis and increase the secretion of neurotrophic factor via activating PI3K/ Akt signaling pathway, thus protecting the loss of dopamine neurons in MPTP-induced PD mice.
Highlights
Network pharmacology approach combined with experimental verification to clarify the mechanism.
Wuzi Yanzong Pill ameliorated MPTP-induced PD mice by activating PI3K/Akt signaling pathway.
Wuzi Yanzong Pill inhibited apoptosis of dopaminergic neurons in MPTP-induced PD mice. |
| doi_str_mv | 10.1007/s11011-022-00993-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2658226522</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2658226522</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-d3f4ab0c00544753e212d8ec00848ddb6a984bffb418a90d418eb212f3b8905b3</originalsourceid><addsrcrecordid>eNp9kM1OGzEQx62KqoS0L9ADssSFi8n4a9d7jPiMSkUOVFUvtby73mCy8Yb1Lig58Rq8Hk9Sh0Ar9cDFI2t-85_RD6GvFI4oQDoKlAKlBBgjAFnGifqABlSmnKQ8kTtoAEpJkooMdtFeCLcAwCXNPqFdLoVSmaAD9Ptnv3b4l_Hrxs_w0tU1Nl1nfW86G_D36fWUOF_2hS3x1LRz50Pjnx-fAj5xwZpg8b0zeDrh30bjeYeDm3lTu02S6W4ezOoz-liZOtgvr3WIfpydXh9fkMur88nx-JIUPJUdKXklTA4FgBQildwyykpl418JVZZ5YjIl8qrKBVUmgzIWm0em4rnKQOZ8iA63ucu2uett6PTChcLWtfG26YNmiVQsPoxF9OA_9Lbp23j2hkoSShVTaaTYliraJoTWVnrZuoVpV5qC3tjXW_s62tcv9rWKQ_uv0X2-sOXfkTfdEeBbIMSWn9n23-53Yv8AenaPhQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2666118287</pqid></control><display><type>article</type><title>Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Hang, Wei ; Fan, Hui-jie ; Li, Yan-rong ; Xiao, Qi ; Jia, Lu ; Song, Li-juan ; Gao, Yao ; Jin, Xiao-ming ; Xiao, Bao-guo ; Yu, Jie-zhong ; Ma, Cun-gen ; Chai, Zhi</creator><creatorcontrib>Hang, Wei ; Fan, Hui-jie ; Li, Yan-rong ; Xiao, Qi ; Jia, Lu ; Song, Li-juan ; Gao, Yao ; Jin, Xiao-ming ; Xiao, Bao-guo ; Yu, Jie-zhong ; Ma, Cun-gen ; Chai, Zhi</creatorcontrib><description>Wuzi Yanzong Pill (WYP) was found to play a protective role on nerve cells and neurological diseases, however the molecular mechanism is unclear. To understand the molecular mechanisms that underly the neuroprotective effect of WYP on dopaminergic neurons in Parkinson’s disease (PD). PD mouse model was induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Gait and hanging tests were used to assess motor behavioral function. Immunofluorescence assay was used to determine TH-positive neurons in substantia nigra (SN). Apoptosis, dopamine and neurotrophic factors as well as expression of PI3K/Akt pathway were detected by TUNEL staining, ELISA and western blotting, respectively. First, it was observed that WYP intervention improved abnormal motor function in MPTP-induced PD model, alleviated the loss of TH
+
neurons in SN, and increased dopamine content in brain, revealing a potential protective effect. Second, network pharmacology was used to analyze the possible targets and pathways of WYP action in the treatment of PD. A total of 126 active components related to PD were screened in WYP, and the related core targets included ALB, GAPDH, Akt1, TP53, IL6 and TNF. Particularly, the effect of WYP on PD may be medicate through PI3K/Akt signaling pathway and apoptotic regulation. The WYP treated PD mice had higher expression of p-PI3K, p-Akt and Bcl-2 but lower expression of Bax and cleaved caspase-3 than the non-WYP treated PD mice. Secretion of brain-derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) were also increased in the treated mice. WYP may inhibit apoptosis and increase the secretion of neurotrophic factor via activating PI3K/ Akt signaling pathway, thus protecting the loss of dopamine neurons in MPTP-induced PD mice.
Highlights
Network pharmacology approach combined with experimental verification to clarify the mechanism.
Wuzi Yanzong Pill ameliorated MPTP-induced PD mice by activating PI3K/Akt signaling pathway.
Wuzi Yanzong Pill inhibited apoptosis of dopaminergic neurons in MPTP-induced PD mice.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-022-00993-8</identifier><identifier>PMID: 35488941</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; 1-Phosphatidylinositol 3-kinase ; AKT protein ; AKT1 protein ; Animals ; Apoptosis ; Bcl-2 protein ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain-derived neurotrophic factor ; Caspase-3 ; Disease Models, Animal ; Dopamine ; Dopamine - metabolism ; Dopamine receptors ; Dopaminergic Neurons ; Drugs, Chinese Herbal - therapeutic use ; Enzyme-linked immunosorbent assay ; Gait ; Glyceraldehyde-3-phosphate dehydrogenase ; Immunofluorescence ; Interleukin 6 ; Metabolic Diseases ; Mice ; Mice, Inbred C57BL ; Molecular modelling ; Movement disorders ; MPTP ; Nerve Growth Factors - metabolism ; Neurodegenerative diseases ; Neurological diseases ; Neurology ; Neurons ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; Oncology ; Original Article ; Parkinson Disease, Secondary - drug therapy ; Parkinson Disease, Secondary - metabolism ; Parkinson's disease ; Pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Signaling ; Substantia Nigra ; Western blotting</subject><ispartof>Metabolic brain disease, 2022-06, Vol.37 (5), p.1435-1450</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-d3f4ab0c00544753e212d8ec00848ddb6a984bffb418a90d418eb212f3b8905b3</citedby><cites>FETCH-LOGICAL-c375t-d3f4ab0c00544753e212d8ec00848ddb6a984bffb418a90d418eb212f3b8905b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11011-022-00993-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-022-00993-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35488941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hang, Wei</creatorcontrib><creatorcontrib>Fan, Hui-jie</creatorcontrib><creatorcontrib>Li, Yan-rong</creatorcontrib><creatorcontrib>Xiao, Qi</creatorcontrib><creatorcontrib>Jia, Lu</creatorcontrib><creatorcontrib>Song, Li-juan</creatorcontrib><creatorcontrib>Gao, Yao</creatorcontrib><creatorcontrib>Jin, Xiao-ming</creatorcontrib><creatorcontrib>Xiao, Bao-guo</creatorcontrib><creatorcontrib>Yu, Jie-zhong</creatorcontrib><creatorcontrib>Ma, Cun-gen</creatorcontrib><creatorcontrib>Chai, Zhi</creatorcontrib><title>Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><addtitle>Metab Brain Dis</addtitle><description>Wuzi Yanzong Pill (WYP) was found to play a protective role on nerve cells and neurological diseases, however the molecular mechanism is unclear. To understand the molecular mechanisms that underly the neuroprotective effect of WYP on dopaminergic neurons in Parkinson’s disease (PD). PD mouse model was induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Gait and hanging tests were used to assess motor behavioral function. Immunofluorescence assay was used to determine TH-positive neurons in substantia nigra (SN). Apoptosis, dopamine and neurotrophic factors as well as expression of PI3K/Akt pathway were detected by TUNEL staining, ELISA and western blotting, respectively. First, it was observed that WYP intervention improved abnormal motor function in MPTP-induced PD model, alleviated the loss of TH
+
neurons in SN, and increased dopamine content in brain, revealing a potential protective effect. Second, network pharmacology was used to analyze the possible targets and pathways of WYP action in the treatment of PD. A total of 126 active components related to PD were screened in WYP, and the related core targets included ALB, GAPDH, Akt1, TP53, IL6 and TNF. Particularly, the effect of WYP on PD may be medicate through PI3K/Akt signaling pathway and apoptotic regulation. The WYP treated PD mice had higher expression of p-PI3K, p-Akt and Bcl-2 but lower expression of Bax and cleaved caspase-3 than the non-WYP treated PD mice. Secretion of brain-derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) were also increased in the treated mice. WYP may inhibit apoptosis and increase the secretion of neurotrophic factor via activating PI3K/ Akt signaling pathway, thus protecting the loss of dopamine neurons in MPTP-induced PD mice.
Highlights
Network pharmacology approach combined with experimental verification to clarify the mechanism.
Wuzi Yanzong Pill ameliorated MPTP-induced PD mice by activating PI3K/Akt signaling pathway.
Wuzi Yanzong Pill inhibited apoptosis of dopaminergic neurons in MPTP-induced PD mice.</description><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</subject><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>AKT1 protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bcl-2 protein</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain-derived neurotrophic factor</subject><subject>Caspase-3</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Dopamine receptors</subject><subject>Dopaminergic Neurons</subject><subject>Drugs, Chinese Herbal - therapeutic use</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gait</subject><subject>Glyceraldehyde-3-phosphate dehydrogenase</subject><subject>Immunofluorescence</subject><subject>Interleukin 6</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular modelling</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neurodegenerative diseases</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Parkinson Disease, Secondary - drug therapy</subject><subject>Parkinson Disease, Secondary - metabolism</subject><subject>Parkinson's disease</subject><subject>Pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Substantia Nigra</subject><subject>Western blotting</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kM1OGzEQx62KqoS0L9ADssSFi8n4a9d7jPiMSkUOVFUvtby73mCy8Yb1Lig58Rq8Hk9Sh0Ar9cDFI2t-85_RD6GvFI4oQDoKlAKlBBgjAFnGifqABlSmnKQ8kTtoAEpJkooMdtFeCLcAwCXNPqFdLoVSmaAD9Ptnv3b4l_Hrxs_w0tU1Nl1nfW86G_D36fWUOF_2hS3x1LRz50Pjnx-fAj5xwZpg8b0zeDrh30bjeYeDm3lTu02S6W4ezOoz-liZOtgvr3WIfpydXh9fkMur88nx-JIUPJUdKXklTA4FgBQildwyykpl418JVZZ5YjIl8qrKBVUmgzIWm0em4rnKQOZ8iA63ucu2uett6PTChcLWtfG26YNmiVQsPoxF9OA_9Lbp23j2hkoSShVTaaTYliraJoTWVnrZuoVpV5qC3tjXW_s62tcv9rWKQ_uv0X2-sOXfkTfdEeBbIMSWn9n23-53Yv8AenaPhQ</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Hang, Wei</creator><creator>Fan, Hui-jie</creator><creator>Li, Yan-rong</creator><creator>Xiao, Qi</creator><creator>Jia, Lu</creator><creator>Song, Li-juan</creator><creator>Gao, Yao</creator><creator>Jin, Xiao-ming</creator><creator>Xiao, Bao-guo</creator><creator>Yu, Jie-zhong</creator><creator>Ma, Cun-gen</creator><creator>Chai, Zhi</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20220601</creationdate><title>Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway</title><author>Hang, Wei ; Fan, Hui-jie ; Li, Yan-rong ; Xiao, Qi ; Jia, Lu ; Song, Li-juan ; Gao, Yao ; Jin, Xiao-ming ; Xiao, Bao-guo ; Yu, Jie-zhong ; Ma, Cun-gen ; Chai, Zhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-d3f4ab0c00544753e212d8ec00848ddb6a984bffb418a90d418eb212f3b8905b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</topic><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>AKT1 protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Bcl-2 protein</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain-derived neurotrophic factor</topic><topic>Caspase-3</topic><topic>Disease Models, Animal</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Dopamine receptors</topic><topic>Dopaminergic Neurons</topic><topic>Drugs, Chinese Herbal - therapeutic use</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gait</topic><topic>Glyceraldehyde-3-phosphate dehydrogenase</topic><topic>Immunofluorescence</topic><topic>Interleukin 6</topic><topic>Metabolic Diseases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular modelling</topic><topic>Movement disorders</topic><topic>MPTP</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neurodegenerative diseases</topic><topic>Neurological diseases</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Parkinson Disease, Secondary - drug therapy</topic><topic>Parkinson Disease, Secondary - metabolism</topic><topic>Parkinson's disease</topic><topic>Pharmacology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Substantia Nigra</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hang, Wei</creatorcontrib><creatorcontrib>Fan, Hui-jie</creatorcontrib><creatorcontrib>Li, Yan-rong</creatorcontrib><creatorcontrib>Xiao, Qi</creatorcontrib><creatorcontrib>Jia, Lu</creatorcontrib><creatorcontrib>Song, Li-juan</creatorcontrib><creatorcontrib>Gao, Yao</creatorcontrib><creatorcontrib>Jin, Xiao-ming</creatorcontrib><creatorcontrib>Xiao, Bao-guo</creatorcontrib><creatorcontrib>Yu, Jie-zhong</creatorcontrib><creatorcontrib>Ma, Cun-gen</creatorcontrib><creatorcontrib>Chai, Zhi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hang, Wei</au><au>Fan, Hui-jie</au><au>Li, Yan-rong</au><au>Xiao, Qi</au><au>Jia, Lu</au><au>Song, Li-juan</au><au>Gao, Yao</au><au>Jin, Xiao-ming</au><au>Xiao, Bao-guo</au><au>Yu, Jie-zhong</au><au>Ma, Cun-gen</au><au>Chai, Zhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2022-06-01</date><risdate>2022</risdate><volume>37</volume><issue>5</issue><spage>1435</spage><epage>1450</epage><pages>1435-1450</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>Wuzi Yanzong Pill (WYP) was found to play a protective role on nerve cells and neurological diseases, however the molecular mechanism is unclear. To understand the molecular mechanisms that underly the neuroprotective effect of WYP on dopaminergic neurons in Parkinson’s disease (PD). PD mouse model was induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Gait and hanging tests were used to assess motor behavioral function. Immunofluorescence assay was used to determine TH-positive neurons in substantia nigra (SN). Apoptosis, dopamine and neurotrophic factors as well as expression of PI3K/Akt pathway were detected by TUNEL staining, ELISA and western blotting, respectively. First, it was observed that WYP intervention improved abnormal motor function in MPTP-induced PD model, alleviated the loss of TH
+
neurons in SN, and increased dopamine content in brain, revealing a potential protective effect. Second, network pharmacology was used to analyze the possible targets and pathways of WYP action in the treatment of PD. A total of 126 active components related to PD were screened in WYP, and the related core targets included ALB, GAPDH, Akt1, TP53, IL6 and TNF. Particularly, the effect of WYP on PD may be medicate through PI3K/Akt signaling pathway and apoptotic regulation. The WYP treated PD mice had higher expression of p-PI3K, p-Akt and Bcl-2 but lower expression of Bax and cleaved caspase-3 than the non-WYP treated PD mice. Secretion of brain-derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) were also increased in the treated mice. WYP may inhibit apoptosis and increase the secretion of neurotrophic factor via activating PI3K/ Akt signaling pathway, thus protecting the loss of dopamine neurons in MPTP-induced PD mice.
Highlights
Network pharmacology approach combined with experimental verification to clarify the mechanism.
Wuzi Yanzong Pill ameliorated MPTP-induced PD mice by activating PI3K/Akt signaling pathway.
Wuzi Yanzong Pill inhibited apoptosis of dopaminergic neurons in MPTP-induced PD mice.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35488941</pmid><doi>10.1007/s11011-022-00993-8</doi><tpages>16</tpages></addata></record> |
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| ispartof | Metabolic brain disease, 2022-06, Vol.37 (5), p.1435-1450 |
| issn | 0885-7490 1573-7365 |
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| subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 1-Phosphatidylinositol 3-kinase AKT protein AKT1 protein Animals Apoptosis Bcl-2 protein Biochemistry Biomedical and Life Sciences Biomedicine Brain Brain-derived neurotrophic factor Caspase-3 Disease Models, Animal Dopamine Dopamine - metabolism Dopamine receptors Dopaminergic Neurons Drugs, Chinese Herbal - therapeutic use Enzyme-linked immunosorbent assay Gait Glyceraldehyde-3-phosphate dehydrogenase Immunofluorescence Interleukin 6 Metabolic Diseases Mice Mice, Inbred C57BL Molecular modelling Movement disorders MPTP Nerve Growth Factors - metabolism Neurodegenerative diseases Neurological diseases Neurology Neurons Neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurosciences Oncology Original Article Parkinson Disease, Secondary - drug therapy Parkinson Disease, Secondary - metabolism Parkinson's disease Pharmacology Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Signaling Substantia Nigra Western blotting |
| title | Wuzi Yanzong pill attenuates MPTP-induced Parkinson’s Disease via PI3K/Akt signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T14%3A35%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Wuzi%20Yanzong%20pill%20attenuates%20MPTP-induced%20Parkinson%E2%80%99s%20Disease%20via%20PI3K/Akt%20signaling%20pathway&rft.jtitle=Metabolic%20brain%20disease&rft.au=Hang,%20Wei&rft.date=2022-06-01&rft.volume=37&rft.issue=5&rft.spage=1435&rft.epage=1450&rft.pages=1435-1450&rft.issn=0885-7490&rft.eissn=1573-7365&rft_id=info:doi/10.1007/s11011-022-00993-8&rft_dat=%3Cproquest_cross%3E2658226522%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2666118287&rft_id=info:pmid/35488941&rfr_iscdi=true |