Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury
The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis wa...
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| Veröffentlicht in: | Molecular medicine reports 2016-12, Vol.14 (6), p.5481-5488 |
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| creator | Gao, Youguang Chen, Ting Lei, Xianghui Li, Yunfeng Dai, Xingui Cao, Yuanyuan Ding, Qionglei Lei, Xiabao Li, Tao Lin, Xianzhong |
| description | The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis was evaluated following induction of focal cerebral ischemia by middle cerebral artery occlusion (MCAO) in rats. PD (30 mg/kg) was administered by caudal vein injection 10 min prior to ischemia/reperfusion (I/R) injury. 24 h following I/R injury, ameliorated modified neurological severity scores (mNSS) and reduced infarct volume were observed in the PD treated group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Annexin V/propidium iodide assays demonstrated the anti-apoptotic effect of PD in the ischemic cortex. In addition, PD improved I/R injury-induced mitochondrial dysfunction, reflected by morphological observations and measurements of mitochondrial membrane potential and intracellular ATP measurement. Western blot analysis revealed an increase in B-cell lymphoma 2 apoptosis regulator (Bcl-2) expression, and a decrease in Bcl-2-associated protein X apoptosis regulator expression in the PD group in comparison with the vehicle treated group. PD treatment also prevented the release of cytochrome c from mitochondria into the cytoplasm, and blunted the activities of caspase-9 and caspase-3. Furthermore, PD treatment decreased the levels of reactive oxygen species in neurons isolated from the ischemic cortex. The findings of this study, therefore, suggest that PD has a dual effect, ameliorating both oxidative stress and mitochondria-dependent apoptosis, making it a promising new therapy for the treatment of ischemic stroke. |
| doi_str_mv | 10.3892/mmr.2016.5936 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5355690</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A479300124</galeid><sourcerecordid>A479300124</sourcerecordid><originalsourceid>FETCH-LOGICAL-c514t-fd268fa56842ac5dcb446ad0f0520b31230275a8e9a84415eedeca1095b2dd393</originalsourceid><addsrcrecordid>eNptkk9vFCEYxidGY2v16NWQeNDLbIGB2eFi0jT-Sxq96Jmw8LLLZgZGYKr9FH5l303rao3hAIHf-_A-8DTNc0ZX3aD4-TTlFaesX0nV9Q-aU7ZWrO0oFQ_v1lyp9UnzpJQ9pb3kUj1uTvh6EFRJddr8_ARLTnNOFWwN10DAe1wVkjyZ03jjTA2RmK0JsVQyhZrsLkWXgxlbBzNEB7ESM6e5phIKQbjugGRTiYUMm2xGYlOu8IP4NI7pe4hbEordwRTMeUaF7JcSUsTK_ZJvnjaPvBkLPLubz5qv795-ufzQXn1-__Hy4qq1konaesf7wRvZD4IbK53dCNEbRz2VnG46xjvK19IMoMwgBJMADqxh6HnDnetUd9a8udWdl80EzqILbFXPOUwm3-hkgr5_EsNOb9O1lp2UvaIo8PpOIKdvC5SqJ7QF42gipKVoNnSKcYadIPryH3SflhzRnmaq42Kt0McfamtG0CH6hPfag6i-QAS_lHGB1Oo_FA6HD2pTBB9w_15Be1tgcyolgz96ZFQfEqQxQfqQIH1IEPIv_n6YI_07Mgi8ugXKbKILLpUjg0otEy3tWykG1v0CYOXSkg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932479568</pqid></control><display><type>article</type><title>Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Gao, Youguang ; Chen, Ting ; Lei, Xianghui ; Li, Yunfeng ; Dai, Xingui ; Cao, Yuanyuan ; Ding, Qionglei ; Lei, Xiabao ; Li, Tao ; Lin, Xianzhong</creator><creatorcontrib>Gao, Youguang ; Chen, Ting ; Lei, Xianghui ; Li, Yunfeng ; Dai, Xingui ; Cao, Yuanyuan ; Ding, Qionglei ; Lei, Xiabao ; Li, Tao ; Lin, Xianzhong</creatorcontrib><description>The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis was evaluated following induction of focal cerebral ischemia by middle cerebral artery occlusion (MCAO) in rats. PD (30 mg/kg) was administered by caudal vein injection 10 min prior to ischemia/reperfusion (I/R) injury. 24 h following I/R injury, ameliorated modified neurological severity scores (mNSS) and reduced infarct volume were observed in the PD treated group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Annexin V/propidium iodide assays demonstrated the anti-apoptotic effect of PD in the ischemic cortex. In addition, PD improved I/R injury-induced mitochondrial dysfunction, reflected by morphological observations and measurements of mitochondrial membrane potential and intracellular ATP measurement. Western blot analysis revealed an increase in B-cell lymphoma 2 apoptosis regulator (Bcl-2) expression, and a decrease in Bcl-2-associated protein X apoptosis regulator expression in the PD group in comparison with the vehicle treated group. PD treatment also prevented the release of cytochrome c from mitochondria into the cytoplasm, and blunted the activities of caspase-9 and caspase-3. Furthermore, PD treatment decreased the levels of reactive oxygen species in neurons isolated from the ischemic cortex. The findings of this study, therefore, suggest that PD has a dual effect, ameliorating both oxidative stress and mitochondria-dependent apoptosis, making it a promising new therapy for the treatment of ischemic stroke.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2016.5936</identifier><identifier>PMID: 27840959</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Annexin V ; Apoptosis ; Apoptosis - drug effects ; Arterial occlusions ; B-cell lymphoma ; Bcl-2 protein ; bcl-2-Associated X Protein - metabolism ; Biomarkers ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Care and treatment ; Carotid arteries ; Caspase ; Caspase-3 ; Caspase-9 ; Cerebral blood flow ; Cerebral cortex ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Cytochrome ; Cytochrome c ; Cytochromes c - metabolism ; Cytoplasm ; Development and progression ; Disease Models, Animal ; DNA nucleotidylexotransferase ; Genetic aspects ; Glucosides - pharmacology ; Health aspects ; Hemorrhage ; Ischemia ; ischemic stroke ; Lymphocytes B ; Male ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial DNA ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; Oxidative stress ; Permeability ; polydatin ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reperfusion ; Reperfusion injury ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Rodents ; Signal Transduction - drug effects ; Stilbenes - pharmacology ; Stroke ; Traumatic brain injury ; Veins & arteries</subject><ispartof>Molecular medicine reports, 2016-12, Vol.14 (6), p.5481-5488</ispartof><rights>Copyright: © Gao et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright: © Gao et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-fd268fa56842ac5dcb446ad0f0520b31230275a8e9a84415eedeca1095b2dd393</citedby><cites>FETCH-LOGICAL-c514t-fd268fa56842ac5dcb446ad0f0520b31230275a8e9a84415eedeca1095b2dd393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,5556,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27840959$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Youguang</creatorcontrib><creatorcontrib>Chen, Ting</creatorcontrib><creatorcontrib>Lei, Xianghui</creatorcontrib><creatorcontrib>Li, Yunfeng</creatorcontrib><creatorcontrib>Dai, Xingui</creatorcontrib><creatorcontrib>Cao, Yuanyuan</creatorcontrib><creatorcontrib>Ding, Qionglei</creatorcontrib><creatorcontrib>Lei, Xiabao</creatorcontrib><creatorcontrib>Li, Tao</creatorcontrib><creatorcontrib>Lin, Xianzhong</creatorcontrib><title>Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis was evaluated following induction of focal cerebral ischemia by middle cerebral artery occlusion (MCAO) in rats. PD (30 mg/kg) was administered by caudal vein injection 10 min prior to ischemia/reperfusion (I/R) injury. 24 h following I/R injury, ameliorated modified neurological severity scores (mNSS) and reduced infarct volume were observed in the PD treated group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Annexin V/propidium iodide assays demonstrated the anti-apoptotic effect of PD in the ischemic cortex. In addition, PD improved I/R injury-induced mitochondrial dysfunction, reflected by morphological observations and measurements of mitochondrial membrane potential and intracellular ATP measurement. Western blot analysis revealed an increase in B-cell lymphoma 2 apoptosis regulator (Bcl-2) expression, and a decrease in Bcl-2-associated protein X apoptosis regulator expression in the PD group in comparison with the vehicle treated group. PD treatment also prevented the release of cytochrome c from mitochondria into the cytoplasm, and blunted the activities of caspase-9 and caspase-3. Furthermore, PD treatment decreased the levels of reactive oxygen species in neurons isolated from the ischemic cortex. The findings of this study, therefore, suggest that PD has a dual effect, ameliorating both oxidative stress and mitochondria-dependent apoptosis, making it a promising new therapy for the treatment of ischemic stroke.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Arterial occlusions</subject><subject>B-cell lymphoma</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biomarkers</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Care and treatment</subject><subject>Carotid arteries</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cerebral blood flow</subject><subject>Cerebral cortex</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Cytochromes c - metabolism</subject><subject>Cytoplasm</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>DNA nucleotidylexotransferase</subject><subject>Genetic aspects</subject><subject>Glucosides - pharmacology</subject><subject>Health aspects</subject><subject>Hemorrhage</subject><subject>Ischemia</subject><subject>ischemic stroke</subject><subject>Lymphocytes B</subject><subject>Male</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial DNA</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxidative stress</subject><subject>Permeability</subject><subject>polydatin</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reperfusion</subject><subject>Reperfusion injury</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Stilbenes - pharmacology</subject><subject>Stroke</subject><subject>Traumatic brain injury</subject><subject>Veins & arteries</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkk9vFCEYxidGY2v16NWQeNDLbIGB2eFi0jT-Sxq96Jmw8LLLZgZGYKr9FH5l303rao3hAIHf-_A-8DTNc0ZX3aD4-TTlFaesX0nV9Q-aU7ZWrO0oFQ_v1lyp9UnzpJQ9pb3kUj1uTvh6EFRJddr8_ARLTnNOFWwN10DAe1wVkjyZ03jjTA2RmK0JsVQyhZrsLkWXgxlbBzNEB7ESM6e5phIKQbjugGRTiYUMm2xGYlOu8IP4NI7pe4hbEordwRTMeUaF7JcSUsTK_ZJvnjaPvBkLPLubz5qv795-ufzQXn1-__Hy4qq1konaesf7wRvZD4IbK53dCNEbRz2VnG46xjvK19IMoMwgBJMADqxh6HnDnetUd9a8udWdl80EzqILbFXPOUwm3-hkgr5_EsNOb9O1lp2UvaIo8PpOIKdvC5SqJ7QF42gipKVoNnSKcYadIPryH3SflhzRnmaq42Kt0McfamtG0CH6hPfag6i-QAS_lHGB1Oo_FA6HD2pTBB9w_15Be1tgcyolgz96ZFQfEqQxQfqQIH1IEPIv_n6YI_07Mgi8ugXKbKILLpUjg0otEy3tWykG1v0CYOXSkg</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Gao, Youguang</creator><creator>Chen, Ting</creator><creator>Lei, Xianghui</creator><creator>Li, Yunfeng</creator><creator>Dai, Xingui</creator><creator>Cao, Yuanyuan</creator><creator>Ding, Qionglei</creator><creator>Lei, Xiabao</creator><creator>Li, Tao</creator><creator>Lin, Xianzhong</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury</title><author>Gao, Youguang ; Chen, Ting ; Lei, Xianghui ; Li, Yunfeng ; Dai, Xingui ; Cao, Yuanyuan ; Ding, Qionglei ; Lei, Xiabao ; Li, Tao ; Lin, Xianzhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-fd268fa56842ac5dcb446ad0f0520b31230275a8e9a84415eedeca1095b2dd393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Arterial occlusions</topic><topic>B-cell lymphoma</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Biomarkers</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Care and treatment</topic><topic>Carotid arteries</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Cerebral blood flow</topic><topic>Cerebral cortex</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Cytochrome</topic><topic>Cytochrome c</topic><topic>Cytochromes c - metabolism</topic><topic>Cytoplasm</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>DNA nucleotidylexotransferase</topic><topic>Genetic aspects</topic><topic>Glucosides - pharmacology</topic><topic>Health aspects</topic><topic>Hemorrhage</topic><topic>Ischemia</topic><topic>ischemic stroke</topic><topic>Lymphocytes B</topic><topic>Male</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial DNA</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oxidative stress</topic><topic>Permeability</topic><topic>polydatin</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reperfusion</topic><topic>Reperfusion injury</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Stilbenes - pharmacology</topic><topic>Stroke</topic><topic>Traumatic brain injury</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Youguang</creatorcontrib><creatorcontrib>Chen, Ting</creatorcontrib><creatorcontrib>Lei, Xianghui</creatorcontrib><creatorcontrib>Li, Yunfeng</creatorcontrib><creatorcontrib>Dai, Xingui</creatorcontrib><creatorcontrib>Cao, Yuanyuan</creatorcontrib><creatorcontrib>Ding, Qionglei</creatorcontrib><creatorcontrib>Lei, Xiabao</creatorcontrib><creatorcontrib>Li, Tao</creatorcontrib><creatorcontrib>Lin, Xianzhong</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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 Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Youguang</au><au>Chen, Ting</au><au>Lei, Xianghui</au><au>Li, Yunfeng</au><au>Dai, Xingui</au><au>Cao, Yuanyuan</au><au>Ding, Qionglei</au><au>Lei, Xiabao</au><au>Li, Tao</au><au>Lin, Xianzhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>14</volume><issue>6</issue><spage>5481</spage><epage>5488</epage><pages>5481-5488</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis was evaluated following induction of focal cerebral ischemia by middle cerebral artery occlusion (MCAO) in rats. PD (30 mg/kg) was administered by caudal vein injection 10 min prior to ischemia/reperfusion (I/R) injury. 24 h following I/R injury, ameliorated modified neurological severity scores (mNSS) and reduced infarct volume were observed in the PD treated group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Annexin V/propidium iodide assays demonstrated the anti-apoptotic effect of PD in the ischemic cortex. In addition, PD improved I/R injury-induced mitochondrial dysfunction, reflected by morphological observations and measurements of mitochondrial membrane potential and intracellular ATP measurement. Western blot analysis revealed an increase in B-cell lymphoma 2 apoptosis regulator (Bcl-2) expression, and a decrease in Bcl-2-associated protein X apoptosis regulator expression in the PD group in comparison with the vehicle treated group. PD treatment also prevented the release of cytochrome c from mitochondria into the cytoplasm, and blunted the activities of caspase-9 and caspase-3. Furthermore, PD treatment decreased the levels of reactive oxygen species in neurons isolated from the ischemic cortex. The findings of this study, therefore, suggest that PD has a dual effect, ameliorating both oxidative stress and mitochondria-dependent apoptosis, making it a promising new therapy for the treatment of ischemic stroke.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27840959</pmid><doi>10.3892/mmr.2016.5936</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Triphosphate - metabolism Animals Annexin V Apoptosis Apoptosis - drug effects Arterial occlusions B-cell lymphoma Bcl-2 protein bcl-2-Associated X Protein - metabolism Biomarkers Brain Ischemia - metabolism Brain Ischemia - pathology Care and treatment Carotid arteries Caspase Caspase-3 Caspase-9 Cerebral blood flow Cerebral cortex Cerebral Cortex - metabolism Cerebral Cortex - pathology Cytochrome Cytochrome c Cytochromes c - metabolism Cytoplasm Development and progression Disease Models, Animal DNA nucleotidylexotransferase Genetic aspects Glucosides - pharmacology Health aspects Hemorrhage Ischemia ischemic stroke Lymphocytes B Male Membrane potential Membrane Potential, Mitochondrial - drug effects Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial DNA Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology Oxidative stress Permeability polydatin Proteins Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion Reperfusion injury Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Rodents Signal Transduction - drug effects Stilbenes - pharmacology Stroke Traumatic brain injury Veins & arteries |
| title | Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury |
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