3,4,5-Tricaffeoylquinic Acid Attenuates Proteasome Inhibition-Mediated Programmed Cell Death in Differentiated PC12 cells
- Authors
- Nam, Yoon Jeong; Lee, Da Hee; Kim, Yun Jeong; Shin, Yong Kyoo; Sohn, Dong Suep; Lee, Min Sung; Lee, Chung Soo
- Issue Date
- Aug-2014
- Publisher
- SPRINGER/PLENUM PUBLISHERS
- Keywords
- 3,4,5-Tricaffeoylquinic acid; Proteasome inhibition; Differentiated PC12 cells; Programmed cell death-related proteins; Protection
- Citation
- NEUROCHEMICAL RESEARCH, v.39, no.8, pp 1416 - 1425
- Pages
- 10
- Journal Title
- NEUROCHEMICAL RESEARCH
- Volume
- 39
- Number
- 8
- Start Page
- 1416
- End Page
- 1425
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/11981
- DOI
- 10.1007/s11064-014-1327-x
- ISSN
- 0364-3190
1573-6903
- Abstract
- The dysfunction of the proteasome system is suggested to be implicated in neuronal degeneration. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. However, the effect of 3,4,5-tricaffeoylquinic acid on the neuronal cell death induced by proteasome inhibition has not been studied. Therefore, in the respect of cell death process, we assessed the effect of 3,4,5-tricaffeoylquinic acid on the proteasome inhibition-induced programmed cell death using differentiated PC12 cells. The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels. Treatment with 3,4,5-tricaffeoylquinic acid attenuated the proteasome inhibitor-induced changes in the programmed cell death-related protein levels, formation of reactive oxygen species, GSH depletion and cell death. The results show that 3,4,5-tricaffeoylquinic acid may attenuate the proteasome inhibitor-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect of 3,4,5-tricaffeoylquinic acid appears to be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
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