Schisandrin B protects PC12 cells by decreasing the expression of amyloid precursor protein and vacuolar protein sorting 35
PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer＇s disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin...
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| Published in | Neural regeneration research Vol. 7; no. 9; pp. 652 - 658 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
India
Medknow Publications & Media Pvt. Ltd
25.03.2012
Department of Neurology, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China%Department of Neurosurgery, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China Medknow Publications & Media Pvt Ltd |
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| Online Access | Get full text |
| ISSN | 1673-5374 1876-7958 |
| DOI | 10.3969/j.issn.1673-5374.2012.09.002 |
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| Abstract | PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer＇s disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. |
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| AbstractList | PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein.PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer＇s disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. R692; PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease.The cells were then treated with 5, 10, and 25 μM Schisandrin B.Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased.Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased.Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change.These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner.This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein.PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease.The cells were then treated with 5, 10, and 25 μM Schisandrin B.Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased.Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased.Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change.These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner.This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer′s disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. Abbreviations: APP, amyloid precursor protein; Aβ, amyloid β-protein; AD, Alzheimer′s disease; VPS35, vacuolar protein sorting 35 |
| Author | Mingmin Yan Shanping Mao Huimin Dong Baohui Liu Qian Zhang Gaofeng Pan Zhiping Fu |
| AuthorAffiliation | Department of Neurology, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China Department of Neurosurgery, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China |
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| Keywords | vacuolar protein sorting 35 Schisandrin B amyloid β-protein 25–35 amyloid precursor protein PC12 cells neural protection amyloid β-protein 25-35 |
| Language | English |
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| Notes | Schisandrin B PC12 cells amyloid β-protein 25-35 amyloid precursor protein vacuolar protein sorting 35 neural protection PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer＇s disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. 11-5422/R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Author contributions: Shanping Mao was responsible for funding. Mingmin Yan was in charge of experimentation, data integration and wrote the final version of the manuscript. Huimin Dong provided information and technology support. Baohui Liu was responsible for data analysis. Gaofeng Pan participated in the study concept and design. Qian Zhang ensured the integrity of data and participated in manuscript authorization. Zhiping Fu was responsible for statistical analysis. Mingmin Yan, Master, Department of Neurology, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China |
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| Publisher | Medknow Publications & Media Pvt. Ltd Department of Neurology, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China%Department of Neurosurgery, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China Medknow Publications & Media Pvt Ltd |
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| References_xml | – reference: 20107219 - N Engl J Med. 2010 Jan 28;362(4):329-44 – reference: 16174740 - Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13461-6 – reference: 19694182 - Pharmazie. 2009 Jul;64(7):450-4 – reference: 15079869 - J Neurosci Res. 2004 May 1;76(3):397-405 – reference: 16628487 - Biogerontology. 2006 Aug;7(4):199-210 – reference: 12349905 - Mol Cell Biochem. 2002 Sep;238(1-2):181-6 – reference: 17646382 - Mol Cell Biol. 2007 Oct;27(19):6842-51 – reference: 16407538 - J Neurosci. 2006 Jan 11;26(2):418-28 – reference: 19038212 - Neuron. 2008 Nov 26;60(4):534-42 – reference: 19900471 - Adv Enzyme Regul. 2010;50(1):216-36 – reference: 1849050 - Chem Biol Interact. 1991;78(1):77-84 – reference: 19625493 - Nucleic Acids Res. 2009 Sep;37(17 ):5678-89 – reference: 10832008 - Neurosci Lett. 2000 Jun 9;286(3):155-8 |
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| Snippet | PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer＇s disease. The cells were then treated with 5, 10, and 25 μM... PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM... PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer′s disease. The cells were then treated with 5, 10, and 25 μM... R692; PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease.The cells were then treated with 5, 10, and... PC12 cell injury was induced using 20 μM amyloid β-protein 25–35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM... |
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| SubjectTerms | Apoptosis Drug dosages Kinases PC12细胞 Protein expression Proteins Research and Report: Traditional Chinese Medicine and Neuroregeneration 五味子乙素 保护 排序 液泡 淀粉样前体蛋白 淀粉样蛋白 逆转录PCR |
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| Title | Schisandrin B protects PC12 cells by decreasing the expression of amyloid precursor protein and vacuolar protein sorting 35 |
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