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Taurine Ameliorates High Glucose Induced Apoptosis in HT-22 Cells

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Taurine 11

Abstract

Diabetes causes memory loss. Hippocampus is responsible for memory and increased apoptosis was found in diabetes patients. Taurine improved memory in diabetes condition. However, mechanism is unclear. In current study, hippocampal cell line HT-22 cells were subjected to analysis as five groups i.e. Control, High glucose (HG) at concentration of 150 mM, HG + 10 mM (T1), 20 mM (T2) and 40 mM (T3) taurine solution. TUNEL assay showed that HG increased the number of apoptotic cell significantly while taurine reduced apoptosis. Taurine increased phosphorylation of Akt in HT-22 cell treated with HG, and increased phosphorylation of Bad (p-Bad) was seen suggesting involvement of Akt/Bad signaling pathway. Expression of Bcl-2 was reduced in HG group but taurine improved this. Bax expression showed opposite trend. This indicated that taurine may reduce apoptosis by controlling balance of Bcl-2 and Bax. When the activation of Akt was blocked by using of perifosine, the effect of taurine disappears either partially or altogether. Thus, it was clear that taurine reduces apoptosis via Akt/Bad pathway in HT-22 cells exposed to HG which further improves downstream balance of Bcl-2 and Bax. This mechanism may be involved in apoptosis of hippocampus cells in diabetic condition.

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Change history

  • 12 October 2019

    Affiliations of authors Muhammad Shahbaz and Shahid Alam were incorrect in the published book. This has now been corrected as below:

Abbreviations

DM:

Diabetes mellitus

MTT:

4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide

HG:

High glucose

TUNEL:

In situ TdT-mediated dUTP nick end labeling

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Acknowledgement

This work was supported by National Natural Science Foundation of China (grant numbers 81501574).

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Wu, P. et al. (2019). Taurine Ameliorates High Glucose Induced Apoptosis in HT-22 Cells. In: Hu, J., Piao, F., Schaffer, S., El Idrissi, A., Wu, JY. (eds) Taurine 11. Advances in Experimental Medicine and Biology, vol 1155. Springer, Singapore. https://doi.org/10.1007/978-981-13-8023-5_75

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