Potentiation of Akt and suppression of caspase-9 activations by electroacupuncture after transient middle cerebral artery occlusion in rats
Electroacupuncture (EA) is an effective curative method for diseases including cerebral ischemia. In the current study, we investigated the effects of EA treatment on the activations of survival Akt and proapoptotic caspase-9 after 90 min of transient middle cerebral artery occlusion (tMCAO) in rat....
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| Veröffentlicht in: | Neuroscience letters 2002-10, Vol.331 (2), p.115-118 |
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| container_title | Neuroscience letters |
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| creator | Wang, Shao Jun Omori, Nobuhiko Li, Feng Jin, Guang Zhang, Wen Ri Hamakawa, Yoshiyuki Sato, Keiko Nagano, Isao Shoji, Mikio Abe, Koji |
| description | Electroacupuncture (EA) is an effective curative method for diseases including cerebral ischemia. In the current study, we investigated the effects of EA treatment on the activations of survival Akt and proapoptotic caspase-9 after 90 min of transient middle cerebral artery occlusion (tMCAO) in rat. Immunoreactivity of phospho-Akt (p-Akt) increased in the ipsilateral hemisphere after tMCAO with a peak at 8 h, and EA enhanced the Akt expression both in the number and the staining strength mainly in the ischemic penumbra (IP) at 8 and 24 h. Cleaved caspase-9 was strongly induced at 8 h in IP, which was suppressed with EA. The number of terminal deoxynucleotidyl transferase-mediated uridine 5′ triphosphate-biotin nick end labelling positive cells reduced at 24 h in the cerebral cortex. These results suggest that EA potentiated the Akt and suppressed the caspase-9 activations, and may have a potential to reduce the number of neuronal cells undergoing apoptotic cell death. |
| doi_str_mv | 10.1016/S0304-3940(02)00866-2 |
| format | Article |
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In the current study, we investigated the effects of EA treatment on the activations of survival Akt and proapoptotic caspase-9 after 90 min of transient middle cerebral artery occlusion (tMCAO) in rat. Immunoreactivity of phospho-Akt (p-Akt) increased in the ipsilateral hemisphere after tMCAO with a peak at 8 h, and EA enhanced the Akt expression both in the number and the staining strength mainly in the ischemic penumbra (IP) at 8 and 24 h. Cleaved caspase-9 was strongly induced at 8 h in IP, which was suppressed with EA. The number of terminal deoxynucleotidyl transferase-mediated uridine 5′ triphosphate-biotin nick end labelling positive cells reduced at 24 h in the cerebral cortex. These results suggest that EA potentiated the Akt and suppressed the caspase-9 activations, and may have a potential to reduce the number of neuronal cells undergoing apoptotic cell death.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/S0304-3940(02)00866-2</identifier><identifier>PMID: 12361854</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Akt ; Animals ; Apoptosis ; Biological and medical sciences ; Caspase 9 ; Caspases - metabolism ; Electroacupuncture ; Immunohistochemistry ; In Situ Nick-End Labeling ; Infarction, Middle Cerebral Artery - enzymology ; Infarction, Middle Cerebral Artery - therapy ; Ischemic Attack, Transient - enzymology ; Ischemic Attack, Transient - therapy ; Male ; Medical sciences ; Miscellaneous ; Phosphatidylinositol 3-Kinases - metabolism ; Prosencephalon - enzymology ; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) ; Rat ; Rats ; Rats, Wistar ; Transient middle cerebral artery occlusion</subject><ispartof>Neuroscience letters, 2002-10, Vol.331 (2), p.115-118</ispartof><rights>2002 Elsevier Science Ireland Ltd</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-1629a66d9b1e725e7f66eeeb72d98868f1e1ed020644dd42bbc20ef33e3ccce53</citedby><cites>FETCH-LOGICAL-c488t-1629a66d9b1e725e7f66eeeb72d98868f1e1ed020644dd42bbc20ef33e3ccce53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0304-3940(02)00866-2$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13949988$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12361854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Shao Jun</creatorcontrib><creatorcontrib>Omori, Nobuhiko</creatorcontrib><creatorcontrib>Li, Feng</creatorcontrib><creatorcontrib>Jin, Guang</creatorcontrib><creatorcontrib>Zhang, Wen Ri</creatorcontrib><creatorcontrib>Hamakawa, Yoshiyuki</creatorcontrib><creatorcontrib>Sato, Keiko</creatorcontrib><creatorcontrib>Nagano, Isao</creatorcontrib><creatorcontrib>Shoji, Mikio</creatorcontrib><creatorcontrib>Abe, Koji</creatorcontrib><title>Potentiation of Akt and suppression of caspase-9 activations by electroacupuncture after transient middle cerebral artery occlusion in rats</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Electroacupuncture (EA) is an effective curative method for diseases including cerebral ischemia. In the current study, we investigated the effects of EA treatment on the activations of survival Akt and proapoptotic caspase-9 after 90 min of transient middle cerebral artery occlusion (tMCAO) in rat. Immunoreactivity of phospho-Akt (p-Akt) increased in the ipsilateral hemisphere after tMCAO with a peak at 8 h, and EA enhanced the Akt expression both in the number and the staining strength mainly in the ischemic penumbra (IP) at 8 and 24 h. Cleaved caspase-9 was strongly induced at 8 h in IP, which was suppressed with EA. The number of terminal deoxynucleotidyl transferase-mediated uridine 5′ triphosphate-biotin nick end labelling positive cells reduced at 24 h in the cerebral cortex. These results suggest that EA potentiated the Akt and suppressed the caspase-9 activations, and may have a potential to reduce the number of neuronal cells undergoing apoptotic cell death.</description><subject>Akt</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Caspase 9</subject><subject>Caspases - metabolism</subject><subject>Electroacupuncture</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Infarction, Middle Cerebral Artery - enzymology</subject><subject>Infarction, Middle Cerebral Artery - therapy</subject><subject>Ischemic Attack, Transient - enzymology</subject><subject>Ischemic Attack, Transient - therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Prosencephalon - enzymology</subject><subject>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Transient middle cerebral artery occlusion</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1q3TAQRkVpaW7SPkKLNi3pwqkk27K8KiGkPxBooO1ayKMxqPW1XY0cuM_Ql47ia5plVgLpzKfhO4y9keJCCqk__hClqIqyrcS5UB-EMFoX6hnbSdOoomkb9Zzt_iMn7JTotxCilnX1kp1IVWpp6mrH_t1OCccUXArTyKeeX_5J3I2e0zLPEYm2a3A0O8Ki5Q5SuFtx4t2B44CQ4uRgmZcR0hKRuz5h5Cm6kULO5vvg_YAcMGIX3cBdzO8HPgEMy5ofRh5dolfsRe8GwtfbecZ-fb7-efW1uPn-5dvV5U0BlTGpkFq1TmvfdhIbVWPTa42IXaN8a4w2vUSJXiihq8r7SnUdKIF9WWIJAFiXZ-z9MXeO098FKdl9IMBhcCNOC9lGycrI8mlQGqOa0pgM1kcQ4kQUsbdzDHsXD1YK-6DLrrrsgwsrlF11WZXn3m4fLN0e_ePU5icD7zbAEbihz51CoEcuB7btusCnI4e5t7uA0RLk7gF9iNmP9VN4YpV7MoG1FA</recordid><startdate>20021011</startdate><enddate>20021011</enddate><creator>Wang, Shao Jun</creator><creator>Omori, Nobuhiko</creator><creator>Li, Feng</creator><creator>Jin, Guang</creator><creator>Zhang, Wen Ri</creator><creator>Hamakawa, Yoshiyuki</creator><creator>Sato, Keiko</creator><creator>Nagano, Isao</creator><creator>Shoji, Mikio</creator><creator>Abe, Koji</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20021011</creationdate><title>Potentiation of Akt and suppression of caspase-9 activations by electroacupuncture after transient middle cerebral artery occlusion in rats</title><author>Wang, Shao Jun ; Omori, Nobuhiko ; Li, Feng ; Jin, Guang ; Zhang, Wen Ri ; Hamakawa, Yoshiyuki ; Sato, Keiko ; Nagano, Isao ; Shoji, Mikio ; Abe, Koji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-1629a66d9b1e725e7f66eeeb72d98868f1e1ed020644dd42bbc20ef33e3ccce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Akt</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Caspase 9</topic><topic>Caspases - metabolism</topic><topic>Electroacupuncture</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Infarction, Middle Cerebral Artery - enzymology</topic><topic>Infarction, Middle Cerebral Artery - therapy</topic><topic>Ischemic Attack, Transient - enzymology</topic><topic>Ischemic Attack, Transient - therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Prosencephalon - enzymology</topic><topic>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. 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In the current study, we investigated the effects of EA treatment on the activations of survival Akt and proapoptotic caspase-9 after 90 min of transient middle cerebral artery occlusion (tMCAO) in rat. Immunoreactivity of phospho-Akt (p-Akt) increased in the ipsilateral hemisphere after tMCAO with a peak at 8 h, and EA enhanced the Akt expression both in the number and the staining strength mainly in the ischemic penumbra (IP) at 8 and 24 h. Cleaved caspase-9 was strongly induced at 8 h in IP, which was suppressed with EA. The number of terminal deoxynucleotidyl transferase-mediated uridine 5′ triphosphate-biotin nick end labelling positive cells reduced at 24 h in the cerebral cortex. These results suggest that EA potentiated the Akt and suppressed the caspase-9 activations, and may have a potential to reduce the number of neuronal cells undergoing apoptotic cell death.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>12361854</pmid><doi>10.1016/S0304-3940(02)00866-2</doi><tpages>4</tpages></addata></record> |
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| subjects | Akt Animals Apoptosis Biological and medical sciences Caspase 9 Caspases - metabolism Electroacupuncture Immunohistochemistry In Situ Nick-End Labeling Infarction, Middle Cerebral Artery - enzymology Infarction, Middle Cerebral Artery - therapy Ischemic Attack, Transient - enzymology Ischemic Attack, Transient - therapy Male Medical sciences Miscellaneous Phosphatidylinositol 3-Kinases - metabolism Prosencephalon - enzymology Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) Rat Rats Rats, Wistar Transient middle cerebral artery occlusion |
| title | Potentiation of Akt and suppression of caspase-9 activations by electroacupuncture after transient middle cerebral artery occlusion in rats |
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