Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway
Objective To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway. Methods S...
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creator | Yao, Jun-peng Feng, Xiu-mei Wang, Lu Li, Yan-qiu Zhu, Zi-yue Yan, Xiang-yun Yang, Yu-qing Li, Ying Zhang, Wei |
description | Objective
To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.
Methods
Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.
Results
The facial functional scores were significantly increased in the EA group than the FNI group (
P |
doi_str_mv | 10.1007/s11655-023-3610-7 |
format | Article |
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To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.
Methods
Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.
Results
The facial functional scores were significantly increased in the EA group than the FNI group (
P
<0.05 or
P
<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (
P
<0.01); however, EA treatment reversed these abnormal changes (
P
<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (
P
<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (
P
<0.05 or
P
<0.01).
Conclusions
EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.]]></description><identifier>ISSN: 1672-0415</identifier><identifier>EISSN: 1993-0402</identifier><identifier>DOI: 10.1007/s11655-023-3610-7</identifier><identifier>PMID: 38212498</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Acupuncture Research ; Medicine ; Medicine & Public Health</subject><ispartof>Chinese journal of integrative medicine, 2024-03, Vol.30 (3), p.251-259</ispartof><rights>The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature 2023</rights><rights>2023. The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c296t-d65e16fd7b5b8d40c5f162a126b17dd1a545b40bd961beb4192c161f97e4d6ea3</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/s11655-023-3610-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11655-023-3610-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38212498$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yao, Jun-peng</creatorcontrib><creatorcontrib>Feng, Xiu-mei</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Li, Yan-qiu</creatorcontrib><creatorcontrib>Zhu, Zi-yue</creatorcontrib><creatorcontrib>Yan, Xiang-yun</creatorcontrib><creatorcontrib>Yang, Yu-qing</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><title>Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway</title><title>Chinese journal of integrative medicine</title><addtitle>Chin. J. Integr. Med</addtitle><addtitle>Chin J Integr Med</addtitle><description><![CDATA[Objective
To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.
Methods
Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.
Results
The facial functional scores were significantly increased in the EA group than the FNI group (
P
<0.05 or
P
<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (
P
<0.01); however, EA treatment reversed these abnormal changes (
P
<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (
P
<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (
P
<0.05 or
P
<0.01).
Conclusions
EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.]]></description><subject>Acupuncture Research</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><issn>1672-0415</issn><issn>1993-0402</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u1DAQxiMEoqXwAFyQj1xCPU7sJMeqdMuKql0t5WzZziTNKokX_9kqr8ET49UWjpxmNN9vvpHmy7KPQL8ApdWlBxCc55QVeSGA5tWr7ByapshpSdnr1IuKpR74WfbO-x2lvBKUv83OipoBK5v6PPt9M6IJzioT93E2ITokG2cnG9CT1XEy2FmNZIvGHtAtRHUBHVkpM6TpPboDkvW8i0kZZrJVwRO9JLqPowrD3JOrGOz-SfULOQyK3H69XxE1t2SzLr5fTo8PW_Jj6NOBI7pR4elZLe-zN50aPX54qRfZz9XN4_W3_O7hdn19dZcb1oiQt4IjiK6tNNd1W1LDOxBMARMaqrYFxUuuS6rbRoBGXULDDAjomgrLVqAqLrLPJ9-9s78i-iCnwRscRzWjjV6yhtU1F4JCQuGEGme9d9jJvRsm5RYJVB6jkKcoZIpCHqOQVdr59GIf9YTtv42_v08AOwE-SXOPTu5sdOkX_j-ufwCcfJWK</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Yao, Jun-peng</creator><creator>Feng, Xiu-mei</creator><creator>Wang, Lu</creator><creator>Li, Yan-qiu</creator><creator>Zhu, Zi-yue</creator><creator>Yan, Xiang-yun</creator><creator>Yang, Yu-qing</creator><creator>Li, Ying</creator><creator>Zhang, Wei</creator><general>Springer Nature Singapore</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20240301</creationdate><title>Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway</title><author>Yao, Jun-peng ; Feng, Xiu-mei ; Wang, Lu ; Li, Yan-qiu ; Zhu, Zi-yue ; Yan, Xiang-yun ; Yang, Yu-qing ; Li, Ying ; Zhang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c296t-d65e16fd7b5b8d40c5f162a126b17dd1a545b40bd961beb4192c161f97e4d6ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acupuncture Research</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yao, Jun-peng</creatorcontrib><creatorcontrib>Feng, Xiu-mei</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Li, Yan-qiu</creatorcontrib><creatorcontrib>Zhu, Zi-yue</creatorcontrib><creatorcontrib>Yan, Xiang-yun</creatorcontrib><creatorcontrib>Yang, Yu-qing</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chinese journal of integrative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yao, Jun-peng</au><au>Feng, Xiu-mei</au><au>Wang, Lu</au><au>Li, Yan-qiu</au><au>Zhu, Zi-yue</au><au>Yan, Xiang-yun</au><au>Yang, Yu-qing</au><au>Li, Ying</au><au>Zhang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway</atitle><jtitle>Chinese journal of integrative medicine</jtitle><stitle>Chin. J. Integr. Med</stitle><addtitle>Chin J Integr Med</addtitle><date>2024-03-01</date><risdate>2024</risdate><volume>30</volume><issue>3</issue><spage>251</spage><epage>259</epage><pages>251-259</pages><issn>1672-0415</issn><eissn>1993-0402</eissn><abstract><![CDATA[Objective
To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.
Methods
Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.
Results
The facial functional scores were significantly increased in the EA group than the FNI group (
P
<0.05 or
P
<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (
P
<0.01); however, EA treatment reversed these abnormal changes (
P
<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (
P
<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (
P
<0.05 or
P
<0.01).
Conclusions
EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.]]></abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><pmid>38212498</pmid><doi>10.1007/s11655-023-3610-7</doi><tpages>9</tpages></addata></record> |
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source | Springer Nature - Complete Springer Journals; Alma/SFX Local Collection |
subjects | Acupuncture Research Medicine Medicine & Public Health |
title | Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway |
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