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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 the expression of Bax and Bcl-2 in HD-exposed PC12 cells. Western blot analysis was used to detect Bax and Bcl-2 (A-C) protein levels. The ratio of Bax/Bcl-2 was analyzed (D). Representatively WB images were shown and quantified data were presented as mean±SD. *p<0.05, compared with control group; #p<0.05, compared with HD group.
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fig_003: Effect of taurine on the expression of Bax and Bcl-2 in HD-exposed PC12 cells. Western blot analysis was used to detect Bax and Bcl-2 (A-C) protein levels. The ratio of Bax/Bcl-2 was analyzed (D). Representatively WB images were shown and quantified data were presented as mean±SD. *p<0.05, compared with control group; #p<0.05, compared with HD group.

Mentions: As taurine suppressed HD-induced apoptosis, we assessed the effects of taurine on the expression levels of Bax and Bcl-2 proteins. As shown in Fig. 3A-C, compared with control group, HD intoxication increased the pro-apoptotic protein expression of Bax in PC12 cells, which was significantly attenuated once HD-intoxicated cells were pretreated with taurine. On the contrary, HD intoxication decreased the anti-apoptotic protein expression of Bcl2 in PC12 cells, which was markedly inhibited once HD-intoxicated cells were pretreated with taurine. It was shown that the ratio of Bax to Bcl-2 (Bax/Bcl-2) determines the susceptibility of a cell to apoptosis5). Bax/Bcl-2 ratio was also assessed in this study. As seen in Fig. 3D, consistent with Bax protein expression, taurine significantly mitigated the elevation of Bax/Bcl-2 ratio induced by HD, indicating that taurine inhibited the disruption of Bax and Bcl-2 expression in HD-treated PC12 cells.Fig. 3.


Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells
Effect of taurine on the expression of Bax and Bcl-2 in HD-exposed PC12 cells. Western blot analysis was used to detect Bax and Bcl-2 (A-C) protein levels. The ratio of Bax/Bcl-2 was analyzed (D). Representatively WB images were shown and quantified data were presented as mean±SD. *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_003: Effect of taurine on the expression of Bax and Bcl-2 in HD-exposed PC12 cells. Western blot analysis was used to detect Bax and Bcl-2 (A-C) protein levels. The ratio of Bax/Bcl-2 was analyzed (D). Representatively WB images were shown and quantified data were presented as mean±SD. *p<0.05, compared with control group; #p<0.05, compared with HD group.
Mentions: As taurine suppressed HD-induced apoptosis, we assessed the effects of taurine on the expression levels of Bax and Bcl-2 proteins. As shown in Fig. 3A-C, compared with control group, HD intoxication increased the pro-apoptotic protein expression of Bax in PC12 cells, which was significantly attenuated once HD-intoxicated cells were pretreated with taurine. On the contrary, HD intoxication decreased the anti-apoptotic protein expression of Bcl2 in PC12 cells, which was markedly inhibited once HD-intoxicated cells were pretreated with taurine. It was shown that the ratio of Bax to Bcl-2 (Bax/Bcl-2) determines the susceptibility of a cell to apoptosis5). Bax/Bcl-2 ratio was also assessed in this study. As seen in Fig. 3D, consistent with Bax protein expression, taurine significantly mitigated the elevation of Bax/Bcl-2 ratio induced by HD, indicating that taurine inhibited the disruption of Bax and Bcl-2 expression in HD-treated PC12 cells.Fig. 3.

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.