Calorie restriction protects against apoptosis, mitochondrial oxidative stress and increased calcium signaling through inhibition of TRPV1 channel in the hippocampus and dorsal root ganglion of rats
Yazarlar (4)
Fatih Gültekin
University Of Health Sciences, Türkiye
Mustafa Nazıroğlu
Süleyman Demirel Üniversitesi, Türkiye
Hasan Basri Savaş
Alanya Alaaddin Keykubat University, Türkiye
Doç. Dr. Bilal ÇİĞ
Süleyman Demirel University, Faculty Of Medicine, Türkiye
| Makale Türü | Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale) | ||
| Dergi Adı | Metabolic Brain Disease | ||
| Dergi ISSN | 0885-7490 Wos Dergi Scopus Dergi | ||
| Dergi Tarandığı Indeksler | SCI | ||
| Makale Dili | İngilizce | Basım Tarihi | 10-2018 |
| Cilt / Sayı / Sayfa | 33 / 5 / 1761–1774 | DOI | 10.1007/s11011-018-0289-0 |
| Makale Linki | http://link.springer.com/10.1007/s11011-018-0289-0 | ||
| Özet |
| The TRPV1 channel is activated in neurons by capsaicin, oxidative stress, acidic pH and heat factors, and these factors are attenuated by the antioxidant role of calorie restriction (CR). Hence, we investigated the hypothesis that the antioxidant roles of CR and food frequency (FF) may modulate TRPV1 activity and apoptosis through inhibition of mitochondrial oxidative stress in hippocampal (HIPPON) and dorsal root ganglion neurons (DRGN). We investigated the contribution of FF and CR to neuronal injury and apoptosis through inhibition of TRPV1 in rats. We assigned rats to control, FF and FF + CR groups. A fixed amount of food ad libitum was supplemented to the control and FF groups for 20 weeks, respectively. FF + CR group were fed the same amount of food as the control group but with 20% less calories during the same period. In major results, TRPV1 currents, intracellular Ca2+ levels, apoptosis, reactive oxygen species, mitochondrial depolarization, PARP-1 expression, caspase 3 and 9 activity and expression values were found to be increased in the HIPPON and DRGN following FF treatment, and these effects were decreased following FF + CR treatment. The FF-induced decrease in cell viability of HIPPO and DRGN, and vitamin E concentration of brain, glutathione peroxidase, vitamin A, and beta-carotene values of the HIPPO, DRGN, plasma, liver and kidney were increased by FF + DR treatment, although lipid peroxidation levels in the same samples were decreased. In conclusion, CR reduces FF-induced increase of oxidative stress, apoptosis and Ca2+ entry through TRPV1 in the HIPPON and DRGN. Our findings may be relevant to the etiology and treatment of obesity following CR treatment. |
| Anahtar Kelimeler |
| Apoptosis | Calorie restriction | Food frequency | Oxidative stress | TRPV1 channel |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları | |
| WoS | 19 |
| SCOPUS | 20 |