| Yazarlar (4) |
Haci Ömer Osmanlıoğlu
Türkiye |
|
Lütfi Yavuz
Türkiye |
Doç. Dr. Bilal ÇİĞ
Kırşehir Ahi Evran Üniversitesi, Türkiye |
|
Mustafa Nazıroğlu
Süleyman Demirel Üniversitesi, Türkiye |
| Özet |
| Sevoflurane is an anesthetic, and it acts on oxidative activity by activating Ca2+ influx. In human neutrophils, oxidative stress activates the voltage-gated calcium channels (VGCC) and the TRPM2 channel; on the other hand, these channels are inhibited by 2-aminoethoxydiphenyl borate (2-APB) and verapamil plus diltiazem (V+D), respectively. Under sevoflurane anesthesia, surgical arthroscopy poses a significant risk to oxidative stress and Ca2+ influx-induced neutrophil infiltration and injury of patients. However, vitamin E may inhibit lipid peroxidation (LP) by upregulating reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) but downregulating TRPM2 and VGCC in the neutrophils of surgical arthroscopy patients. This topic was examined in the current study. We enrolled 20 patients in the current study, separating them into two primary groups: patients and patients plus vitamin E. Ten patients were divided into two groups: preoperative (N1) and postoperative (N2), both of which were not given vitamin E therapy. The remaining ten patients were given 300 IU of vitamin E two hours prior to their surgical arthroscopy (E1), and their blood was again drawn following the procedure (E2). Prior to fMLP stimulation, the isolated neutrophils from each of the four groups were incubated with 10 µM V+D and 100 µM 2-APB. In the neutrophils, there was an increase in intracellular free Ca2+ ([Ca2+]i) concentration and LP levels due to the downregulation of GSH and GSH-Px; however, following vitamin E treatment, GSH concentration and GSH-Px activity increased in the E2 group. While 2-APB and V+D treatment reduced the concentration of [Ca2+]i in the neutrophils, vitamin E administration had no effect on this measurement. In summary, vitamin E treatment mitigated the GSH and GSH-Px alterations induced by I/R damage, while TRPM2 and VGCC inhibition reduced the [Ca2+]i rise induced by I/R injury. One potential treatment approach for I/R-induced oxidative neutrophil damage is the suppression of TRPM2 and VGCC. |
| Anahtar Kelimeler |
| Ischemia/reperfusion injury | Neutrophil | Sevoflurane | TRPM2 channel | Vitamin E |
| Makale Türü | Özgün Makale |
| Makale Alt Türü | SCOPUS dergilerinde yayımlanan tam makale |
| Dergi Adı | Journal of Cellular Neuroscience and Oxidative StressThis link is disabled., |
| Dergi ISSN | 2149-7222 Scopus Dergi |
| Dergi Tarandığı Indeksler | Scopus |
| Makale Dili | İngilizce |
| Basım Tarihi | 12-2024 |
| Cilt No | 16 |
| Sayı | 2 |
| Sayfalar | 1205 / 1213 |
| Doi Numarası | 10.37212/jcnos.1569027 |
| Makale Linki | https://dergipark.org.tr/en/pub/jcnos/issue/87741/1569027 |
| Atıf Sayıları |
