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Fırat Üniversitesi Sağlık Bilimleri Tıp Dergisi
2014, Cilt 28, Sayı 1, Sayfa(lar) 025-028
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Effect of Cilostazol on KCl and Capsaicin Induced Increase in Intracellular Calcium Signaling in Rat Sensory Neurons
Oktay BURMA1, Mete ÖZCAN2, Emine KAÇAR3, Ayhan UYSAL1, Selim KUTLU4
1Fırat Üniversitesi, Tıp Fakültesi, Kalp ve Damar Cerrahi Anabilim Dalı, Elazığ, TÜRKİYE
2Fırat Üniversitesi, Tıp Fakültesi, Biyofizik Anabilim Dalı, Elazığ, TÜRKİYE
3Fırat Üniversitesi, Tıp Fakültesi, Fizyoloji Anabilim Dalı, Elazığ, TÜRKİYE
4Necmettin Erbakan Üniversitesi, Meram Tıp Fakültesi, Fizyoloji Anabilim Dalı, Konya, TÜRKİYE

Objective: Cilostazol, a specific cAMP phosphodiesterase III inhibitor, is used for medical treatment of intermittent claudication in peripheral artery disease to prevent leg pain during physical activity. Dorsal root ganglion (DRG) neurons are eligible experimental model for pain investigations. Aim of this study was to figure out the effect of cilostazol on intracellular calcium ([Ca2+i) signaling in cultured rat DRG neurons.

Materials and Methods: DRG neurons were grown in primary culture following enzymatic and mechanical dissociation of ganglia from 2-day-old Wistar rats. DRG neuronal cultures were loaded with 1μmol Fura-2AM and [Ca2+i responses to stimulation were assessed by using fluorescent ratiometry. Cultured cells were excited at 340 and 380nm and emission was recorded at 510nm. Responses were determined by the change in 340/380 ratio (basal-peak) for individual neurons. After basal recordings, KCl (30mM) and capcaicin (1μM) applied to medium for induction of [Ca2+]i. Cilostazol treated alone or co-administered with KCl and capcaicin for determining the possible changes in calcium signaling in small size DRG neurons. Data were analyzed by using Student's t test, P level of <0.05 defining statistical significance.

Results: Firstly exposure to cilostazol failed to cause any significant change in basal [Ca2+i response (basal=100.0±0.0 and cilostazol =99.8±0.8 %). KCl and capcaicin had significant increase in [Ca2+i responses to 190.3±6.2% and 165.6±4.1% (respectively, P< 0.001). But coapplication of cilostazol with KCl and capcaicin did not alter the KCl and capcaicin induced elevation in [Ca2+i (189.4 ±% 4.6 and 166.0 ± 3.8% respectively).

Conclusion: In conclusion, the results of present study suggest that cilostazol has no effect on [Ca2+i signaling in rat sensory neurons in vitro. It seems cilostazol may activate other mechanism(s) at cellular level rather than modulating calcium signaling in DRG neurons.

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