- Tytuł:
- THE EFFECTS OF CARVACROL ON OXIDATIVE STRESS PARAMETERS AND APOPTOSIS PROCESS VIA TRPA1 CHANNELS IN NEUROBLASTOMA CELLS
- Autorzy:
-
Gunal, Mehmet Y.
Ovey, Ishak S. - Powiązania:
- https://bibliotekanauki.pl/articles/895278.pdf
- Data publikacji:
- 2019-06-28
- Wydawca:
- Polskie Towarzystwo Farmaceutyczne
- Tematy:
-
apoptosis
caspase-3
ROS
neuroblastoma
carvacrol - Opis:
- Objectives: This study is a preliminary study to investigate the effects of carvacrol (CRV) obtained from thyme on the apoptosis process in neuroblastoma cells. Methods: In this study, seven groups were designed as control, CRV, CRV + AP-18, CRV + melatonin, CRV + melatonin + AP-18, melatonin and melatonin + AP-18. All groups were stimulated using CNM (cinnamaldehyde) which is TRPA1 channel stimulator. Levels of Reactive oxygen species (ROS), caspase-3, caspase-9, mitochondrial depolarization, apoptosis, intracellular free calcium and 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) were measured. Data were evaluated using one way ANOVA analysis. Results: Levels of ROS, mitochondrial depolarisation, caspase-3 and -9 and apoptosis were significantly higher in all groups treated with CRV compared to control (P <0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, ROS and caspase-3 were significantly lower than control (P <0,05). MTT levels were significantly decreased in all groups treated with CRV compared to control (P <0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, MTT was higher than control(P <0,05). Conclusion: It has also been shown that CRV can also exert its effects through TRPA1 channels in neuroblastoma cells, which may accelerate the apoptosis process by acting on these channels, increasing ROS and caspase-3 levels. Changes in MTT levels support this result. However, in order to better evaluate the effects of CRV on the apoptosis process, it would be useful to investigate changes in caspase-9, mitochondrial depolarization, and calcium channels.
- Źródło:
-
Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 3; 535-542
0001-6837
2353-5288 - Pojawia się w:
- Acta Poloniae Pharmaceutica - Drug Research
- Dostawca treści:
- Biblioteka Nauki
Artykuł