- 학회지
권호별 검색
- 현재 페이지 경로
-
- HOME
- 학회지
- 학회지
- 권호별 검색
| Original Article | |||||
| Dementia and Neurocognitive Disorders 2017: 16: 3: 64-71 | |||||
| Candesartan Restores the Amyloid Beta-Inhibited Proliferation of Neural Stem Cells by Activating the Phosphatidylinositol 3-Kinase Pathway | |||||
|---|---|---|---|---|---|
| Hojin Choi Na-Young Choi Kyu-Yong Lee Young Joo Lee Seong-Ho Koh | |||||
| Department of Neurology, Hanyang University Guri Hospital, Guri, Korea | |||||
| Candesartan Restores the Amyloid Beta-Inhibited Proliferation of Neural Stem Cells by Activating the Phosphatidylinositol 3-Kinase Pathway | |||||
| Hojin Choi Na-Young Choi Kyu-Yong Lee Young Joo Lee Seong-Ho Koh | |||||
| Department of Neurology, Hanyang University Guri Hospital, Guri, Korea | |||||
| Background: and Purpose Neurogenesis in the adult brain is important for memory and learning, and the alterations in neural stem cells (NSCs) may be an important aspect of Alzheimer’s disease (AD) pathogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway has been suggested to have an important role in neuronal cell survival and is highly involved in adult neurogenesis. Candesartan is an angiotensin II receptor antagonist used for the treatment of hypertension and several studies have reported that it also has some neuroprotective effects. We investigated whether candesartan could restore the amyloid-β(25–35) (Aβ25-35) oligomer-inhibited proliferation of NSCs by focusing on the PI3K pathway. Methods: To evaluate the effects of candesartan on the Aβ25-35 oligomer-inhibited proliferation of NSCs, the NSCs were treated with several concentrations of candesartan and/or Aβ25-35 oligomers, and MTT assay and trypan blue staining were performed. To evaluate the effect of candesartan on the Aβ-inhibited proliferation of NSCs, we performed a bromodeoxyuridine (BrdU) labeling assay. The levels of p85α PI3K, phosphorylated Akt (pAkt) (Ser473), phosphorylated glycogen sinthase kinase-3β (pGSK-3β)(Ser9), and heat shock transcription factor-1 (HSTF- 1) were analyzed by Western blotting. Results: The BrdU assays demonstrated that NSC proliferation decreased with Aβ25-35 oligomer treatment; however, a combined treatment with candesartan restored it. Western blotting displayed that candesartan treatment increased the expression levels of p85α PI3K, pAkt (Ser473), pGSK-3β (Ser9), and HSTF. The NSCs were pretreated with a PI3K inhibitor, LY294002; the effects of candesartan on the proliferation of NSCs inhibited by Aβ25-35 oligomers were almost completely blocked. Conclusions Together, these results suggest that candesartan restores the Aβ25-35 oligomer-inhibited proliferation of NSCs by activating the PI3K pathway. |
|||||
| Key Words: candesartan, amyloid beta, neural stem cells. | |||||
| 대한치매학회지 (Dementia and Neurocognitive Disorders) | |||||
- Sponsor
-
- Tel : +82-2-587-7462
- Fax : +82-2-587-7482
- e-mail : secretkda@thedementia.co.kr
- 사업자등록번호 : 214-82-63838
- 상호 : 대한치매학회
- 대표자명 : 양동원 이사장
Copyright © The Korean Dementia Association, All rights reserved