| The protective effect of trihexyphenidyl on the beta-amyloid peptide (25-35)-induced cytotoxicity in PC12 cells. | |
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MedLine Citation:
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PMID: 20101432 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In the development and progression of Alzheimer's disease (AD), β-amyloid peptide (Aβ) that induced cytotoxicity containing apoptosis and excess production of reactive oxygen species (ROS) is considered as a causal role. The aim of present study is to investigate the protective effect of Trihexyphenidyl (THY) on Aβ(25-35)-induced cytotoxicity in cultured rat pheochromocytoma (PC12) cells. In this report, the cell survival was measured by MTT assay, the enzyme activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), the contents of lipid peroxidation products malondialdehyde (MDA) and ROS in the cells were determined. Acridine orange (AO) was used to observe the morphological characteristic of apoptotic cells. Mitochondrial membrane potential in PC12 cells were monitored by fluorospectrophotometer combining with Rh123. As a cell permeable fluorescent probe, Fura-2/AM was employed to detect intracellular [Ca(2+)]. The results showed that after incubation with Aβ(25-35) (10 μM) for 24 h, there were decreased changes in cell viability, SOD, and GSH-PX activity as well as mitochondrial membrane potential, in contrast, the levels of [Ca(2+)](i), ROS, and MDA were increased, THY significantly attenuated all the changes induced by Aβ(25-35), indicating that THY exhibited protective effect against Aβ(25-35)-induced cytotoxicity, which may represent the cellular mechanisms of the action. |
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Authors:
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Zhen-Zhen Liu; Bian-Sheng Ji |
Publication Detail:
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Type: Journal Article Date: 2010-01-26 |
Journal Detail:
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Title: Clinical and experimental medicine Volume: 10 ISSN: 1591-9528 ISO Abbreviation: Clin. Exp. Med. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-10-25 Completed Date: 2011-01-31 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100973405 Medline TA: Clin Exp Med Country: Italy |
Other Details:
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Languages: eng Pagination: 237-43 Citation Subset: IM |
Affiliation:
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Key Laboratory of Natural Medicine and Immune Engineering, Henan University, 475001, Kaifeng, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amyloid beta-Peptides
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antagonists & inhibitors*,
toxicity* Animals Antimetabolites / pharmacology* Calcium / analysis Cell Survival / drug effects Cytosol / chemistry Glutathione Peroxidase / metabolism Malondialdehyde / analysis Membrane Potential, Mitochondrial / drug effects PC12 Cells Peptide Fragments / antagonists & inhibitors*, toxicity* Rats Reactive Oxygen Species / analysis Superoxide Dismutase / metabolism Tetrazolium Salts / metabolism Thiazoles / metabolism Trihexyphenidyl / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Peptides; 0/Antimetabolites; 0/Peptide Fragments; 0/Reactive Oxygen Species; 0/Tetrazolium Salts; 0/Thiazoles; 0/amyloid beta-protein (25-35); 144-11-6/Trihexyphenidyl; 298-93-1/thiazolyl blue; 542-78-9/Malondialdehyde; 7440-70-2/Calcium; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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