Anti-tumor Necrosis Factor Alpha (Infliximab) Attenuates Apoptosis, Oxidative Stress, and Calcium Ion Entry Through Modulation of Cation Channels in Neutrophils of Patients with Ankylosing Spondylitis
Yazarlar (4)
Süleyman Demirel Üniversitesi, Türkiye
Süleyman Demirel Üniversitesi, Türkiye
Süleyman Demirel Üniversitesi, Türkiye
Doç. Dr. Mehmet AYKUR
Tokat Gaziosmanpaşa Üniversitesi, Türkiye
| Makale Türü | Özgün Makale |
| Makale Alt Türü | SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale |
| Dergi Adı | Journal of Membrane Biology |
| Dergi ISSN | 0022-2631 Wos Dergi Scopus Dergi |
| Dergi Tarandığı Indeksler | SCI-Expanded |
| Dergi Grubu | Q3 |
| Makale Dili | İngilizce |
| Basım Tarihi | 08-2016 |
| Cilt No | 249 |
| Sayı | 4 |
| Sayfalar | 437 / 447 |
| DOI Numarası | 10.1007/s00232-016-9884-3 |
| Makale Linki | http://dx.doi.org/10.1007/s00232-016-9884-3 |
| Özet |
| Ankylosing Spondylitis (AS) is known to be associated with increased neutrophil activation and oxidative stress, however, the mechanism of neutrophil activation is still unclear. We have hypothesized that the antioxidant and anti-tumor necrosis factor properties of infliximab may affect intracellular Ca2+ concentration in the neutrophils of AS patients. The objective of this study was to investigate the effects of infliximab on calcium signaling, oxidative stress, and apoptosis in neutrophils of AS patients. Neutrophils collected from ten patients with AS and ten healthy controls were used in the study. In a cell viability test, the ideal non-toxic dose and incubation time of infliximab were found as 100 μM and 1 h, respectively. In some experiments, the neutrophils were incubated with the voltage-gated calcium channel (VGCC) blockers verapamil + diltiazem (V + D) and the TRPM2 channel blocker 2-aminoethyl diphenylborinate (2-APB). Intracellular Ca2+ concentration, lipid peroxidation, apoptosis, caspase 3, and caspase 9 values were high in neutrophils of AS patients and were reduced with infliximab treatment. Reduced glutathione level and glutathione peroxidase activity were low in the patients and increased with infliximab treatment. The intracellular Ca2+ concentrations were low in 2-APB and V + D groups. In conclusion, the current study suggests that infliximab is useful against apoptotic cell death and oxidative stress in neutrophils of patients with AS, which seem to be dependent on increased levels of intracellular Ca2+ through activation of TRPM2 and VGCC. |
| Anahtar Kelimeler |
| Ankylosing spondylitis | Apoptosis | Calcium signaling | Infliximab | Neutrophil | Oxidative stress |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları | |
| WoS | 10 |
| SCOPUS | 14 |
| Google Scholar | 22 |