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

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.


The viability of PC12 cells received HD alone or with taurine. A. Dose- and time-dependent effect of HD on cell viability. PC12 cells were exposed to different concentrations (5, 10, 20, 40 mM) of HD for 0, 6, 12 and 24 h; B. PC12 cells were treated with different concentrations of taurine (0–100 mM) for 30 min, followed by 20 mM HD for 24 h. Cell viability was assessed by MTT assay. Each column represents mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.
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fig_001: The viability of PC12 cells received HD alone or with taurine. A. Dose- and time-dependent effect of HD on cell viability. PC12 cells were exposed to different concentrations (5, 10, 20, 40 mM) of HD for 0, 6, 12 and 24 h; B. PC12 cells were treated with different concentrations of taurine (0–100 mM) for 30 min, followed by 20 mM HD for 24 h. Cell viability was assessed by MTT assay. Each column represents mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.

Mentions: To determining the dose and time necessary for HD to induce maximum cellular damage, we carried out the dose and time dependent assays by MTT. As evidenced from Fig. 1A, HD intoxication decreased the cell viability linearly up to a dose of 20 mM for 24 h in a dose- and time-dependent. This dose and time were, therefore, chosen as the optimum dose and time of HD throughout the study.Fig. 1.


Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells
The viability of PC12 cells received HD alone or with taurine. A. Dose- and time-dependent effect of HD on cell viability. PC12 cells were exposed to different concentrations (5, 10, 20, 40 mM) of HD for 0, 6, 12 and 24 h; B. PC12 cells were treated with different concentrations of taurine (0–100 mM) for 30 min, followed by 20 mM HD for 24 h. Cell viability was assessed by MTT assay. Each column represents 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_001: The viability of PC12 cells received HD alone or with taurine. A. Dose- and time-dependent effect of HD on cell viability. PC12 cells were exposed to different concentrations (5, 10, 20, 40 mM) of HD for 0, 6, 12 and 24 h; B. PC12 cells were treated with different concentrations of taurine (0–100 mM) for 30 min, followed by 20 mM HD for 24 h. Cell viability was assessed by MTT assay. Each column represents mean±SD, n=6. *p<0.05, compared with control group; #p<0.05, compared with HD group.
Mentions: To determining the dose and time necessary for HD to induce maximum cellular damage, we carried out the dose and time dependent assays by MTT. As evidenced from Fig. 1A, HD intoxication decreased the cell viability linearly up to a dose of 20 mM for 24 h in a dose- and time-dependent. This dose and time were, therefore, chosen as the optimum dose and time of HD throughout the study.Fig. 1.

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.