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P1‐469: The Protective Effect of Compound of CTS and RKG on Beta‐Amyloid Protein‐induced Apoptosis in PC12 Cells
Author(s) -
Ying Liu Yuan
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.08.014
Subject(s) - lactate dehydrogenase , apoptosis , chemistry , programmed cell death , cell , pharmacology , caspase 3 , mtt assay , microbiology and biotechnology , medicine , biochemistry , enzyme , biology
Background:Theprotective effect of a Japanese herbalmedicine,Compound of Chotosan (CTS) and Rokumi-gan (RKG) (CTS and RKG, Tsumura., Tokyo, Japan)were investigated on b-Amyloid protein (b40) -induced apoptosis in PC12 cells.Methods:Two biochemical methods, determination of the lactate dehydrogenase (LDH) release and activity of 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) reduction of cells, were used. We evaluated the caspase-3 activity of the compound of CTS and RKG on b40-induced apoptosis in PC12 cells using a fluorophotometer (Type 850, HITACHI).Results:Compound of CTS and RKG significantly inhibited the increase in LDH release following b40-induced cell injury and significantly increasedMTTreduction, significantly increasing the cell survival rate. These results suggested the protective effects of compound of CTS and RKG. In addition, the inhibition of b40-induced cell injury and the significant increase in the cell survival rate bycompoundofCTSandRKGwerecontinuous, suggesting continuous protective effects. Compound of CTS and RKG significantly inhibited caspase-3 activation due to b40-induced cell injury. Conclusions: In summary, the administration of compound of CTS and RKG increased the cell survival rate, which suggested its protective effects on neurons. Compound of CTS and RKG significantly inhibitedb40-induced cell injury, which suggested its protective effects against neuron injury. Compound of CTS and RKG inhibited b40-induced neuron death, and a pathway