The role of oxidative stress in the protective effect of boric acid against glutamate excitotoxicity in C6 glioma cells

Öz

This study designed to investigate the biochemical changes in glial cells' oxidant/antioxidant systems in response to glutamate-induced excitotoxicity of boric acid (BA). The present study employed C6 glial cells. For the study, cells were separated into 4 groups as control, glutamate (10mM), glutamate+BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL), and BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL). The control group was not treated. The cells in the glutamate group were treated with 10 mM glutamate for 24 hours. BA was administered one hour prior to the addition of glutamate and incubated for 24 hours. The viability of the cells was evaluated using an XTT assay. Commercial kits were used for biochemical analyses. Significance was set at less than 0.05. The biochemical analysis revealed that the levels of malondialdehyde (MDA), nitric oxide (NO), inducible nitric oxide snythase (iNOS), neuronal nitric oxide synthase (nNOS), and total oxidant status (TOS) were elevated in the glutamate group compared to the control group (p<0.05). It was detemined that BA treatment resulted in a statistically significant reduction in these levels compared to the glutamate group. (p<0.05). The levels of SOD and TAS were found to decrease in the glutamate group and to increase with BA pretreatment (p<0.05). The results demonstrated that BA exhibited protective effects on glial cells against glutamate exposure. Furthermore, BA was observed to exert its neuroprotective effect by increasing the antioxidant defense mechanism and reducing oxidative and nitrosative stress.

Anahtar Kelimeler

• Boric Acid
• C6 Cells
• Glutamate Excitotoxicity
• Oxidative Stress

Borik asidin C6 glioma hücrelerinde glutamat eksitotoksisitesine karşı koruyucu etkinliğinde oksidatif stresin rolü

Öz

Bu çalışma, borik asidin (BA) glutamat ile indüklenen eksitotoksisiteye karşı glial hücrelerde meydana gelen oksidan/antioksidan sistem değişikliklerini biyokimyasal olarak incelemek amacıyla tasarlanmıştır. Bu çalışmada C6 glial hücreleri kullanılmıştır. Hücreler kontrol, glutamat (10mM), glutamat+BA(0,23; 0,46; 0,93; 1,87 ve 3,75 μg/mL) ve BA (0,23; 0,46; 0,93; 1,87 ve 3,75 μg/ml) olmak üzere 4 gruba ayrılmıştır. Kontrol grubuna herhangi bir tedavi yapılmamıştır. Glutamat grubundaki hücreler 24 saat boyunca 10 mM glutamat ile muamele edilmiştir. BA ise glutamat eklenmeden 1 saat önce verildi ve 24 saat boyunca inkübe edilmiştir. Hücre canlılığı XTT testi ile ölçülmüştür. Biyokimyasal analizler için ticari kitler kullanılmıştır. Anlamlılık 0.05’ten küçük olarak kabul edilmiştir. Biyokimyasal analiz ile glutamat grubunda malondialdehit (MDA), nitrik oksit (NO), indüklenmiş nitrik oksit sentaz (iNOS), nöronal nitrik oksit sentaz (nNOS) ve toplam oksidant (TOS) seviyelerinin kontrol grubuna göre arttığı (p<0,05), BA ön tedavisi ile glutamat grubuna göre istatistiksel olarak azaldığı tespit edilmiştir (p<0,05). SOD ve TAS seviyesi glutamat grubunda azalırken BA ön tedavisi ile artmıştır (p<0,05). BA, glial hücreler üzerinde glutamat maruziyetine karşı koruyucu etkiler göstermiştir. Bu nöroprotektif etkiyi antioksidan savunma mekanizmasını artırarak, oksidatif ve nitrozatif stresi azaltarak oluşturmuştur.

Anahtar Kelimeler

• Borik Asit
• C6 Hücreleri
• Glutamat Eksitotoksisitesi
• Oksidatif Stres

Kaynakça

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