Quipazine treatment exacerbates oxidative stress in glutamate-induced HT-22 neuronal cells

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Yıldızhan K., Öztürk A.

THE EUROPEAN RESEARCH JOURNAL, vol.8, no.4, pp.521-528, 2022 (Peer-Reviewed Journal)

  • Publication Type: Article / Article
  • Volume: 8 Issue: 4
  • Publication Date: 2022
  • Doi Number: 10.18621/eurj.1027423
  • Journal Indexes: EMBASE, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.521-528
  • Van Yüzüncü Yıl University Affiliated: Yes


Objectives: Quipazine is a serotonin agonist. It is known that serotonin, an important neurotransmitter, contributes to the etiology of psychiatric and many neurodegenerative diseases. However, the effect of the serotonin agonist quipazine on HT-22 cells in glutamate-induced cytotoxicity is unknown. This study aims to investigate the effect of quipazine on increased oxidative stress (OS) as a result of glutamate-induced cytotoxicity in HT-22 cells.

Methods: The cells were divided into 4 groups, Control group: no treatment was applied, Glutamate group: glutamate was incubated at 10 mM for 24 h, Quipazine group: incubated with different doses of quipazine for 24 h, Quipazine+Glutamate group were pre-treated with various concentrations (25, 50, 100 and 200 µM) of quipazine for 1 h and then exposed to 10 mM glutamate for 24 h. Cell viability rate between groups was measured by the XTT assay. OS and antioxidant levels were measured with the Total Oxidant Status (TOS) and Total Antioxidant Status (TAS) Elisa kits, and Caspase-3 levels were also examined in caspase activity. 

Results: Quipazine at different concentrations showed significant differences in cell viability in HT-22 cells. An appropriate dose of 25 µM was accepted for quipazine in the study. Quipazine treatment with glutamate-toxicity in the cells further reduced TAS levels and significantly increased TOS levels. It was also observed that the Caspase-3 level increased more in the Quipazine + Glutamate group according to the Glutamate group. 

Conclusions: The results determined that the use of quipazine is an agent that will further increase the neurodegeneration caused by glutamate toxicity.