Inhibitory Effect of Flavonoid Luteolin on 6-Hydroxydopamine Cytotoxicity via Suppression of Apoptosis-Related Protein Activation.
- Author:
Seon Wha LEE
1
;
Jin Ho KANG
;
Jeong Ho HAN
;
Doo Eung KIM
;
Chung Soo LEE
Author Information
1. Department of Neurology, Veterans Health Service Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
6-Hydroxydopamine;
Apoptosis-related proteins;
Flavonoid luteolin;
PC12 cells;
Protective effect;
Reactive oxygen species
- MeSH:
Animals;
Apoptosis;
Caspases;
Cell Death;
Cytochromes c;
Hypogonadism;
Luteolin;
Mitochondrial Diseases;
Neurons;
Ophthalmoplegia;
Oxidative Stress;
Oxidopamine;
Parkinson Disease;
PC12 Cells;
Reactive Oxygen Species
- From:Journal of the Korean Neurological Association
2012;30(4):284-292
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Flavonoid luteolin has been shown to exhibit cell protective effect. However, it is still uncertain whether the effect of luteolin on cellular toxicity of the parkinsonian toxin 6-hydroxydopamine is mediated by apoptosis-related protein activation. METHODS: In differentiated PC12 cells exposed to 6-hydroxydopamine in combination with luteolin, we observed the apoptosis-related protein activation, nuclear damage, formation of reactive oxygen species and cell death. RESULTS: 6-Hydroxydopamine caused apoptosis by inducing a decrease in Bid, Bcl-2, Bcl-xL and survivin levels, increase in Bax levels, cytochrome c release and activation of caspases. Treatment with luteolin reduced changes in the apoptosis-related protein levels, formation of reactive oxygen species, nuclear damage and cell death. CONCLUSIONS: Luteolin may reduce the 6-hydroxydopamine-induced apoptosis in differentiated PC12 cells by suppressing the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The preventive effect of luteolin may be associated with its inhibitory effect on the production of reactive oxygen species. Luteolin may attenuate the oxidative stress and mitochondrial dysfunction-induced neuronal cell death take place in Parkinson's disease.
