Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 류제일 | - |
dc.date.accessioned | 2020-09-21T08:33:00Z | - |
dc.date.available | 2020-09-21T08:33:00Z | - |
dc.date.issued | 2019-10 | - |
dc.identifier.citation | SCIENTIFIC REPORTS, v. 9, article no. 15717 | en_US |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://www.nature.com/articles/s41598-019-52083-y | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/154038 | - |
dc.description.abstract | Amlodipine, a L-type calcium channel blocker, has been reported to have a neuroprotective efect in brain ischemia. Mitochondrial calcium overload leads to apoptosis of cells in neurologic diseases. We evaluated the neuroprotective efects of amlodipine camsylate (AC) on neural stem cells (NSCs) injured by oxygen glucose deprivation (OGD) with a focus on mitochondrial structure and function. NSCs were isolated from rodent embryonic brains. Efects of AC on cell viability, proliferation, level of free radicals, and expression of intracellular signaling proteins were assessed in OGD-injured NSCs. We also investigated the efect of AC on mitochondrial structure in NSCs under OGD by transmission electron microscopy. AC increased the viability and proliferation of NSCs. This benefcial efect of AC was achieved by strong protection of mitochondria. AC markedly enhanced the expression of mitochondrial biogenesis-related proteins and mitochondrial anti-apoptosis proteins. Together, our results indicate that AC protects OGD-injured NSCs by protecting mitochondrial structure and function. The results of the present study provide insight into the mechanisms underlying the protective efects of AC on NSCs. | en_US |
dc.description.sponsorship | This research was supported by the Basic Science Research Program of the National Research Foundation of Korea, which is funded by the Ministry of Science, ICT, and Future Planning (2018R1D1A1A09082825, 2018R1A2A2A15023219, and 2018R1D1A1B07047722), by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI18C1254), and by the Medical Research Center (2017R1A5A2015395). | en_US |
dc.language.iso | en | en_US |
dc.publisher | NATURE PUBLISHING GROUP | en_US |
dc.subject | NEURONAL CELL-DEATH | en_US |
dc.subject | PERMEABILITY TRANSITION | en_US |
dc.subject | OXIDATIVE STRESS | en_US |
dc.subject | CHANNEL BLOCKER | en_US |
dc.subject | REGULATORS | en_US |
dc.subject | ISCHEMIA | en_US |
dc.subject | RECOVERY | en_US |
dc.subject | BESYLATE | en_US |
dc.subject | CA2+ | en_US |
dc.title | Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylate | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1038/s41598-019-52083-y | - |
dc.relation.page | 1-11 | - |
dc.relation.journal | SCIENTIFIC REPORTS | - |
dc.contributor.googleauthor | Park, Hyun-Hee | - |
dc.contributor.googleauthor | Han, Myung-Hoon | - |
dc.contributor.googleauthor | Choi, Hojin | - |
dc.contributor.googleauthor | Lee, Young Joo | - |
dc.contributor.googleauthor | Kim, Jae Min | - |
dc.contributor.googleauthor | Cheong, Jin Hwan | - |
dc.contributor.googleauthor | Ryu, Je Il | - |
dc.contributor.googleauthor | Lee, Kyu-Yong | - |
dc.contributor.googleauthor | Koh, Seong-Ho | - |
dc.relation.code | 2019002548 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | ryujeil | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.