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Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells

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ABSTRACT

2,5-hexanedione (HD) is the ultimate neurotoxic metabolite of hexane, causing the progression of nerve diseases in human. It was reported that HD induced apoptosis and oxidative stress. Taurine has been shown to be a potent antioxidant. In the present study, we investigated the protection of taurine against HD-induced apoptosis in PC12 cells and the underlying mechanism. Our results showed the decreased viability and increased apoptosis in HD-exposed PC12 cells. HD also induced the disturbance of Bax and Bcl-2 expression, the loss of MMP, the release of mitochondrial cytochrome c and caspase-3 activation in PC12 cells. Moreover, HD resulted in an increase in reactive oxygen species (ROS) level and a decline in the activities of superoxidedismutase and catalase in PC12 cells. However, taurine pretreatment ameliorated the increased apoptosis and the alterations in key regulators of mitochondria-dependent pathway in PC12 exposed to HD. The increased ROS level and the decreased activities of the antioxidant enzymes in HD group were attenuated by taurine. These results indicate that pretreatment of taurine may, at least partly, prevent HD-induced apoptosis via inhibiting mitochondria-dependent pathway. It is also suggested that the potential of taurine against HD-induced apoptosis may benefit from its anti-oxidative property.

No MeSH data available.


Effect of taurine on caspase-3 activity in HD-exposed PC12 cells. Data were presented as mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.
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fig_006: Effect of taurine on caspase-3 activity in HD-exposed PC12 cells. Data were presented as mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.

Mentions: Caspase-3 is the effector of mitochondria-mediated apoptosis pathway. In the present study, the effect of taurine on the activity of caspase-3 protein in PC12 cells was shown in Fig. 6. As expected, compared with control group, a significant increase in caspase-3 activity was observed in HD-intoxicated PC12 cells, which was significantly repressed once HD-intoxicated cells were pretreated with taurine, suggesting that HD-induced caspase-3 activation was prevented by taurine.Fig. 6.


Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells
Effect of taurine on caspase-3 activity in HD-exposed PC12 cells. Data were presented as mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig_006: Effect of taurine on caspase-3 activity in HD-exposed PC12 cells. Data were presented as mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.
Mentions: Caspase-3 is the effector of mitochondria-mediated apoptosis pathway. In the present study, the effect of taurine on the activity of caspase-3 protein in PC12 cells was shown in Fig. 6. As expected, compared with control group, a significant increase in caspase-3 activity was observed in HD-intoxicated PC12 cells, which was significantly repressed once HD-intoxicated cells were pretreated with taurine, suggesting that HD-induced caspase-3 activation was prevented by taurine.Fig. 6.

View Article: PubMed Central - PubMed

ABSTRACT

2,5-hexanedione (HD) is the ultimate neurotoxic metabolite of hexane, causing the progression of nerve diseases in human. It was reported that HD induced apoptosis and oxidative stress. Taurine has been shown to be a potent antioxidant. In the present study, we investigated the protection of taurine against HD-induced apoptosis in PC12 cells and the underlying mechanism. Our results showed the decreased viability and increased apoptosis in HD-exposed PC12 cells. HD also induced the disturbance of Bax and Bcl-2 expression, the loss of MMP, the release of mitochondrial cytochrome c and caspase-3 activation in PC12 cells. Moreover, HD resulted in an increase in reactive oxygen species (ROS) level and a decline in the activities of superoxidedismutase and catalase in PC12 cells. However, taurine pretreatment ameliorated the increased apoptosis and the alterations in key regulators of mitochondria-dependent pathway in PC12 exposed to HD. The increased ROS level and the decreased activities of the antioxidant enzymes in HD group were attenuated by taurine. These results indicate that pretreatment of taurine may, at least partly, prevent HD-induced apoptosis via inhibiting mitochondria-dependent pathway. It is also suggested that the potential of taurine against HD-induced apoptosis may benefit from its anti-oxidative property.

No MeSH data available.