{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:10:52Z","timestamp":1787008252213,"version":"build-2736575974"},"reference-count":41,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2014,6,1]],"date-time":"2014-06-01T00:00:00Z","timestamp":1401580800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Rejuvenation Research"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:p>\n                    Parkinson's disease is a neurodegenerative disorder characterized by progressive and selective death of dopaminergic neurons. Understanding the neuroprotective effects of chemical reagents has attracted increasing attention. The \u03bc opioid agonist morphine exerts both toxic and protective effects. However, until recently, the neuroprotective role of morphine against 6-hydroxydopamine (6-OHDA)\u2013induced cell death has not been studied. Here, we investigated the effects of morphine on 6-OHDA\u2013induced neurotoxicity in human neuroblastoma SH-SY5Y cell line as an\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    model of Parkinson's disease. Cell damage was induced by 150\u2009\u03bcM 6-OHDA, and the cells' viability was examined by MTT assay. Intracellular calcium, reactive oxygen species (ROS), and mitochondrial membrane potential were determined by the fluorescence spectrophotometry method. Fragmented DNA and biochemical markers of apoptosis were also determined by gel electrophoresis and immunoblotting, respectively. The data showed that 6-OHDA caused a loss of cell viability and mitochondrial membrane potential. In addition, intracellular ROS and calcium levels, activated caspase-3, Bax:Bcl-2 ratio, cytochrome\n                    <jats:italic toggle=\"yes\">c<\/jats:italic>\n                    release, as well as DNA fragmentation were significantly increased in 6-OHDA\u2013treated cells. Incubation of SH-SY5Y cells with morphine (100\u2009\u03bcM) elicited a protective effect and reduced biochemical markers of cell damage and death. These results suggest that morphine has neuroprotective effects against 6-OHDA\u2013induced neurotoxicity, and such effects are accompanied by its anti-oxidant, calcium blocking, and anti-apoptotic properties.\n                  <\/jats:p>","DOI":"10.1089\/rej.2013.1473","type":"journal-article","created":{"date-parts":[[2013,12,16]],"date-time":"2013-12-16T12:50:02Z","timestamp":1387198202000},"page":"255-263","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":36,"title":["Morphine Protects SH-SY5Y Human Neuroblastoma Cells Against 6-Hydroxydopamine\u2013Induced Cell Damage: Involvement of Anti-Oxidant, Calcium Blocking, and Anti-Apoptotic Properties"],"prefix":"10.1177","volume":"17","author":[{"given":"Leila","family":"Elyasi","sequence":"first","affiliation":[{"name":"Kerman University of Medical Sciences. Kerman","place":["Iran"]},{"name":"Kerman University of Medical Sciences. Kerman","place":["Iran"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seyed Hassan","family":"Eftekhar-Vaghefi","sequence":"additional","affiliation":[{"name":"Kerman University of Medical Sciences. Kerman","place":["Iran"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saeed","family":"Esmaeili-Mahani","sequence":"additional","affiliation":[{"name":"Shahid Bahonar University of Kerman. Kerman","place":["Iran"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2014,6]]},"reference":[{"key":"e_1_3_3_2_2","first-page":"61","article-title":"Advances in the mechanisms of Parkinson's disease","volume":"15","author":"Tolleson CM","year":"2013","unstructured":"Tolleson CM, , Fang JY. Advances in the mechanisms of Parkinson's disease. 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