Establishment of Human Neuroblastoma Cell-Line (SK-N-SH) as an In Vitro Model of Morphine Addiction

查看全文 作　　者：Noor Azuin [1]Suliman;Noor Azlina Abu [1]Bakar;Mohamad Aris Mohd [2]Moklas;Che Norma Mat [2]Taib 机构地区：[1]Faculty of Medicine and Health Science,Universiti Sultan Zainal Abidin(UniSZA),Kampus Kota,Jalan Sultan Mahmud,Kuala Terengganu20400,Malaysia;[2]Department of Biomedical Sciences,Faculty of Medicine and Health Sciences,Universiti Putra Malaysia,43400 UPM Serdang,Selangor,Malaysia 出　　处：《Journal of Pharmacy and Pharmacology》索引2021年第9卷第3期,共7页 摘　　要：Morphine is a schedule II-controlled substance that used to allow the diminution of intra-operative, post-operative orchronic pain. However, its usage is limited due to addiction and overdose liabilities. Morphine was observed to cause tolerance,dependence and withdrawal in human. Justification: to date lack of scientific evidence of morphine addiction was carried out byusing specific single human neuroblastoma cell-line (SK-N-SH). Therefore, this study was performed to establish the morphineaddiction model in this cell line. The cells were exposed to morphine for 24 hrs before treatment with methadone, as ananti-withdrawal drug for subsequence 24 hours. The cytosolic fraction of the cell was used in different objectives including receptoraffinity, withdrawal properties, endocytic machinery, desensitisation or internalisation and cellular adaptation. The result shows thatmorphine and methadone bind to the μ-opioid receptor. The morphine-treated cells were observed to increase the expression ofaddiction markers, have a low rate of the endocytic machinery, cause desensitisation of receptor and reduce cellular adaptation.Those changes by morphine were normalised by the treatment of methadone. As a whole, it is postulated that neuroblastoma cell line,SK-N-SH, can be used as an in-vitro model to demonstrate morphine addiction before animal and human testing. 关 键 词：Morphine addiction receptor affinity withdrawal properties endocytic machinery desensitisation internalisation cellular adaptation methadone.