Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson’s Disease: Modulation of Mitochondrial Perturbations
The recent emergence of ursodeoxycholic acid (UDCA) as a contender in modifying neurotoxicity in human dopaminergic cells as well as its recognized anti-apoptotic and anti-inflammatory potentials in various hepatic pathologies raised impetus in investigating its anti-parkinsonian effect in rat roten...
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| Veröffentlicht in: | Molecular neurobiology 2016-03, Vol.53 (2), p.810-817 |
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| creator | Abdelkader, Noha F. Safar, Marwa M. Salem, Hesham A. |
| description | The recent emergence of ursodeoxycholic acid (UDCA) as a contender in modifying neurotoxicity in human dopaminergic cells as well as its recognized anti-apoptotic and anti-inflammatory potentials in various hepatic pathologies raised impetus in investigating its anti-parkinsonian effect in rat rotenone model. UDCA prominently improved motor performance in the open field test and halted the decline in the striatal dopamine content. Meanwhile, it improved mitochondrial function as verified by elevation of ATP associated with preservation of mitochondrial integrity as portrayed in the electron microscope examination. In addition, through its anti-inflammatory potential, UDCA reduced the rotenone-induced nuclear factor-κB expression and tumor necrosis factor alpha level. Furthermore, UDCA amended alterations in Bax and Bcl-2 and reduced the activities of caspase-8, caspase-9, and caspase-3, indicating that it suppressed rotenone-induced apoptosis via modulating both intrinsic and extrinsic pathways. In conclusion, UDCA can be introduced as a novel approach for the management of Parkinson’s disease via anti-apoptotic and anti-inflammatory mechanisms. These effects are probably linked to dopamine synthesis and mitochondrial regulation. |
| doi_str_mv | 10.1007/s12035-014-9043-8 |
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UDCA prominently improved motor performance in the open field test and halted the decline in the striatal dopamine content. Meanwhile, it improved mitochondrial function as verified by elevation of ATP associated with preservation of mitochondrial integrity as portrayed in the electron microscope examination. In addition, through its anti-inflammatory potential, UDCA reduced the rotenone-induced nuclear factor-κB expression and tumor necrosis factor alpha level. Furthermore, UDCA amended alterations in Bax and Bcl-2 and reduced the activities of caspase-8, caspase-9, and caspase-3, indicating that it suppressed rotenone-induced apoptosis via modulating both intrinsic and extrinsic pathways. In conclusion, UDCA can be introduced as a novel approach for the management of Parkinson’s disease via anti-apoptotic and anti-inflammatory mechanisms. 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UDCA prominently improved motor performance in the open field test and halted the decline in the striatal dopamine content. Meanwhile, it improved mitochondrial function as verified by elevation of ATP associated with preservation of mitochondrial integrity as portrayed in the electron microscope examination. In addition, through its anti-inflammatory potential, UDCA reduced the rotenone-induced nuclear factor-κB expression and tumor necrosis factor alpha level. Furthermore, UDCA amended alterations in Bax and Bcl-2 and reduced the activities of caspase-8, caspase-9, and caspase-3, indicating that it suppressed rotenone-induced apoptosis via modulating both intrinsic and extrinsic pathways. In conclusion, UDCA can be introduced as a novel approach for the management of Parkinson’s disease via anti-apoptotic and anti-inflammatory mechanisms. These effects are probably linked to dopamine synthesis and mitochondrial regulation.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Behavior, Animal - drug effects</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspases - metabolism</subject><subject>Cell Biology</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Enzymes</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Male</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - ultrastructure</subject><subject>Neostriatum - drug effects</subject><subject>Neostriatum - enzymology</subject><subject>Neostriatum - metabolism</subject><subject>Neostriatum - pathology</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurons - ultrastructure</subject><subject>Neurosciences</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson's disease</subject><subject>Rats, Wistar</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rotenone</subject><subject>Ursodeoxycholic Acid - pharmacology</subject><issn>0893-7648</issn><issn>1559-1182</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>eNp1kcFqFTEUhoNY7LX6AG4k4MbNaJJJMom7y1VrocUidh0ymTM2dW5yTTJgdz6AL9DX80ma6a0igquz-L_znwMfQs8oeUUJ6V5nykgrGkJ5owlvG_UAragQuqFUsYdoRZRum05ydYge53xFCGOUdI_QIROCMC7ZCv28SDkOEL9fu8s4eYfXzg94vYXJx2QLZLzexV2JpUYbm50dAPuAyyXgT7FAiAHwWS2YcBzxuU1ffcgx_Ppxk_Fbn8FmeLPk82SLj2GBznyJ9VYYkrcTPodU5tTfpfkJOhjtlOHp_TxCF-_ffd58aE4_Hp9s1qeNE5yWpqNa6haY5lINANZSsAS4JMqRHiRTSijZi6EfpOCjHbXmbiTKyp4BOMrbI_Ry37tL8dsMuZitzw6myQaIcza0k0p0XHSsoi_-Qa_inEL9bqG44ppqUim6p1yKOScYzS75rU3XhhKzqDJ7VaaqMosqo-rO8_vmud_C8Gfjt5sKsD2QaxS-QPrr9H9bbwHkEqGY</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Abdelkader, Noha F.</creator><creator>Safar, Marwa M.</creator><creator>Salem, Hesham A.</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>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20160301</creationdate><title>Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson’s Disease: Modulation of Mitochondrial Perturbations</title><author>Abdelkader, Noha F. ; Safar, Marwa M. ; Salem, Hesham A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-719693e29468deeaa1ea0e4608c0be6288586b5dbd654faf994cf08a6b2eec143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Behavior, Animal - drug effects</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspases - metabolism</topic><topic>Cell Biology</topic><topic>Disease Models, Animal</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Enzymes</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Male</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - ultrastructure</topic><topic>Neostriatum - drug effects</topic><topic>Neostriatum - enzymology</topic><topic>Neostriatum - metabolism</topic><topic>Neostriatum - pathology</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neurons - ultrastructure</topic><topic>Neurosciences</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson's disease</topic><topic>Rats, Wistar</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rotenone</topic><topic>Ursodeoxycholic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abdelkader, Noha F.</creatorcontrib><creatorcontrib>Safar, Marwa M.</creatorcontrib><creatorcontrib>Salem, Hesham A.</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>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>Engineering Research Database</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>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abdelkader, Noha F.</au><au>Safar, Marwa M.</au><au>Salem, Hesham A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson’s Disease: Modulation of Mitochondrial Perturbations</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>53</volume><issue>2</issue><spage>810</spage><epage>817</epage><pages>810-817</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>The recent emergence of ursodeoxycholic acid (UDCA) as a contender in modifying neurotoxicity in human dopaminergic cells as well as its recognized anti-apoptotic and anti-inflammatory potentials in various hepatic pathologies raised impetus in investigating its anti-parkinsonian effect in rat rotenone model. UDCA prominently improved motor performance in the open field test and halted the decline in the striatal dopamine content. Meanwhile, it improved mitochondrial function as verified by elevation of ATP associated with preservation of mitochondrial integrity as portrayed in the electron microscope examination. In addition, through its anti-inflammatory potential, UDCA reduced the rotenone-induced nuclear factor-κB expression and tumor necrosis factor alpha level. Furthermore, UDCA amended alterations in Bax and Bcl-2 and reduced the activities of caspase-8, caspase-9, and caspase-3, indicating that it suppressed rotenone-induced apoptosis via modulating both intrinsic and extrinsic pathways. In conclusion, UDCA can be introduced as a novel approach for the management of Parkinson’s disease via anti-apoptotic and anti-inflammatory mechanisms. These effects are probably linked to dopamine synthesis and mitochondrial regulation.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25502462</pmid><doi>10.1007/s12035-014-9043-8</doi><tpages>8</tpages></addata></record> |
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| subjects | Adenosine Triphosphate - metabolism Animals Apoptosis Apoptosis - drug effects Behavior, Animal - drug effects Biomedical and Life Sciences Biomedicine Caspases - metabolism Cell Biology Disease Models, Animal Dopamine Dopamine - metabolism Enzymes Gene Expression Regulation - drug effects Male Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - ultrastructure Neostriatum - drug effects Neostriatum - enzymology Neostriatum - metabolism Neostriatum - pathology Neurobiology Neurology Neurons - drug effects Neurons - metabolism Neurons - pathology Neurons - ultrastructure Neurosciences Parkinson Disease - metabolism Parkinson Disease - pathology Parkinson's disease Rats, Wistar RNA, Messenger - genetics RNA, Messenger - metabolism Rotenone Ursodeoxycholic Acid - pharmacology |
| title | Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson’s Disease: Modulation of Mitochondrial Perturbations |
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