Özet:

Objective Hypoxia is among the most important factors regarding to neuronal injury. TRPM7 cation channels, which are expressed in neurons, and it is well known that TRPM7 channels are activated by many factors including hypoxia and cellular pH changes. Therefore, in this study, it was aimed to investigate the effect of carvacrol, a potent inhibitor of TRPM7 cation channels, on cellular survival and apoptotic parameters in an in vitro hypoxia model induced by cobalt chloride (CoCl2), which is frequently used to do hypoxia in experimental studies. Material and Method The SH-SY5Y cells were grown in cell culture flasks. Cells were incubated for 24 hours with medium containing 200 μM CoCl2 to induction of hypoxia. In the group, in which the effect of carvacrol was tested, the cells were incubated with a medium containing carvacrol (250 μM) for 1 h to TRPM7 channel inhibition, and the incubation was completed by applying hypoxia for 24 h. Then, the cells detached from the culture flasks and apoptosis test, MTT cell viability analysis, reactive oxygen species (ROT) production determination, mitochondrial membrane depolarization (MMD) determination and caspase 3, 8 and 9 enzyme activities were performed. Results It was demonstrated that while cell viability decreased in the hypoxia-induced group compared to the control, there was an increase in other parameters (apoptosis, ROS production, MMD and caspase activities) that reduced to cell viability. It was observed that the parameters reducing cellular viability were significantly decreased in the hypoxia-treated group upon carvacrol pre-incubation compared to the CoCl2 group. Conclusion Carvacrol administration can be slowed down to abnormal cellular damage and cell death mechanisms caused by hypoxic conditions. It is thought that the positive effects of carvacrol in SH-SY5Y cells, whose TRPM7 cation channel expression is well known, are mediated by mostly TRPM7 channels.

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