Neuroprotective effect of D-Psicose on 6-hydroxydopamine-induced apoptosis in rat pheochromocytoma (PC12) cells

Maki K. Takata; Fuminori Yamaguchi; Koichi Nakanose; Yasuo Watanabe; Naoya Hatano; Ikuko Tsukamoto; Mitsuhiro Nagata; Ken Izumori; Masaaki Tokuda

doi:10.1263/jbb.100.511

Neuroprotective effect of D-Psicose on 6-hydroxydopamine-induced apoptosis in rat pheochromocytoma (PC12) cells

Maki K. Takata, Fuminori Yamaguchi, Koichi Nakanose, Yasuo Watanabe, Naoya Hatano, Ikuko Tsukamoto, Mitsuhiro Nagata, Ken Izumori, Masaaki Tokuda

Research output: Contribution to journal › Article

51 Citations (Scopus)

Abstract

We evaluated the neuroprotective effects of D-psicose, one of the rare sugars, on 6-hydroxydopamine (6-OHDA)-induced apoptosis in catecholaminergic PC12 cells, the in vitro model of Parkinson's disease (PD). Apoptotic characteristics of PC12 cells were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling (TUNEL) assay. The results showed that D-psicose at a concentration of 50 mM, exerted significant protective effects against the 6-OHDA (200 μM)-induced PC12 cell apoptosis, while other sugars had little or no protective effects. We have observed a significant increase in the level of intracellular glutathione after 24 h in 6-OHDA (200 μM) treated cells, while a decrease in the level was observed at 3 h and 6 h. Also, a synergistic exposure to D-psicose and 6-OHDA for 24 h showed a significant increase in intracellular glutathione level. Therefore, these results suggest that D-psicose may play a potential role as a neuroprotective agent in the treatment of neurodegenerative diseases by inducing an up-regulation of intracellular glutathione.

Original language	English
Pages (from-to)	511-516
Number of pages	6
Journal	Journal of Bioscience and Bioengineering
Volume	100
Issue number	5
DOIs	https://doi.org/10.1263/jbb.100.511
Publication status	Published - 2005
Externally published	Yes

Keywords

6-hydroxydopamine (6-OHDA)
Antioxidant
Apoptosis
D-psicose
PC12 cells
Parkinson's disease (PD)
Rare sugars

ASJC Scopus subject areas

Biotechnology
Bioengineering
Applied Microbiology and Biotechnology

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Takata, M. K., Yamaguchi, F., Nakanose, K., Watanabe, Y., Hatano, N., Tsukamoto, I., Nagata, M., Izumori, K., & Tokuda, M. (2005). Neuroprotective effect of D-Psicose on 6-hydroxydopamine-induced apoptosis in rat pheochromocytoma (PC12) cells. Journal of Bioscience and Bioengineering, 100(5), 511-516. https://doi.org/10.1263/jbb.100.511

Neuroprotective effect of D-Psicose on 6-hydroxydopamine-induced apoptosis in rat pheochromocytoma (PC12) cells. / Takata, Maki K.; Yamaguchi, Fuminori; Nakanose, Koichi; Watanabe, Yasuo; Hatano, Naoya; Tsukamoto, Ikuko; Nagata, Mitsuhiro; Izumori, Ken; Tokuda, Masaaki.

In: Journal of Bioscience and Bioengineering, Vol. 100, No. 5, 2005, p. 511-516.

Research output: Contribution to journal › Article

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abstract = "We evaluated the neuroprotective effects of D-psicose, one of the rare sugars, on 6-hydroxydopamine (6-OHDA)-induced apoptosis in catecholaminergic PC12 cells, the in vitro model of Parkinson's disease (PD). Apoptotic characteristics of PC12 cells were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling (TUNEL) assay. The results showed that D-psicose at a concentration of 50 mM, exerted significant protective effects against the 6-OHDA (200 μM)-induced PC12 cell apoptosis, while other sugars had little or no protective effects. We have observed a significant increase in the level of intracellular glutathione after 24 h in 6-OHDA (200 μM) treated cells, while a decrease in the level was observed at 3 h and 6 h. Also, a synergistic exposure to D-psicose and 6-OHDA for 24 h showed a significant increase in intracellular glutathione level. Therefore, these results suggest that D-psicose may play a potential role as a neuroprotective agent in the treatment of neurodegenerative diseases by inducing an up-regulation of intracellular glutathione.",

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