Yilmaz, Selcuk, Gur, Cihan, Kucukler, Sefa, Akaras, Nurhan, Kandemir, Fatih. (1403). Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-κB, Caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway. , 27(4), 485-491. doi: 10.22038/ijbms.2023.74088.16094
Selcuk Yilmaz; Cihan Gur; Sefa Kucukler; Nurhan Akaras; Fatih Mehmet Kandemir. "Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-κB, Caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway". , 27, 4, 1403, 485-491. doi: 10.22038/ijbms.2023.74088.16094
Yilmaz, Selcuk, Gur, Cihan, Kucukler, Sefa, Akaras, Nurhan, Kandemir, Fatih. (1403). 'Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-κB, Caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway', , 27(4), pp. 485-491. doi: 10.22038/ijbms.2023.74088.16094
Yilmaz, Selcuk, Gur, Cihan, Kucukler, Sefa, Akaras, Nurhan, Kandemir, Fatih. Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-κB, Caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway. , 1403; 27(4): 485-491. doi: 10.22038/ijbms.2023.74088.16094

Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-κB, Caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway

Iranian Journal of Basic Medical Sciences
مقاله 11، دوره 27، شماره 4، تیر 2024، صفحه 485-491    اصل مقاله (630.27 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.74088.16094
نویسندگان
Selcuk Yilmaz1؛ Cihan Gur* 2؛ Sefa Kucukler2؛ Nurhan Akaras3؛ Fatih Mehmet Kandemir4
1Department of Orthopedics and Traumatology, Faculty of Medicine, Kütahya Health Sciences University, Kütahya, Turkey
2Department of Biochemistry, Faculty of Veterinary Medicine, Atatürk University, Erzurum, Turkey
3Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Turkey
4Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Turkey
چکیده
Objective(s): In the present study, the potential protective effects of zingerone (ZNG) against sciatic nerve damage caused by sodium arsenite (SA), a common environmental pollutant, were evaluated by various biochemical, molecular, and histological methods.
Materials and Methods: In the study, SA and ZNG were given to 35 male Sprague Dawley rats for 14 days. At the end of the period, the sciatic nerve tissues were taken and the markers involved in oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis were analyzed.
Results: The data obtained showed that SA decreased glutathione (GSH) levels and increased malondialdehyde (MDA) levels in the sciatic nerve tissue. However, it was determined that these markers approached the control group levels due to the anti-oxidant properties of ZNG. While SA triggered endoplasmic reticulum stress and apoptosis pathways, ZNG suppressed them. Moreover, SA up-regulated inflammatory markers such as nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1β), and neuronal nitric oxide synthases (nNOS) in the sciatic nerves and caused neuro-inflammation and inhibited cell survival by suppressing serine/threonine-protein kinase 2 (Akt2) and forkhead box protein O1 (FOXO1) genes. It has also been shown histopathologically that SA causes degeneration in the sciatic nerves. In contrast, ZNG suppressed neuro-inflammation, activated Akt2/FOXO1 signaling, and repaired histological irregularities.
Conclusion: In general, SA caused oxidative stress, inflammation, ER stress, and apoptosis in the sciatic nerves of rats, causing damage to the tissues, however, ZNG suppressed these pathways and protected the sciatic nerves from the destructive effect of SA.
کلیدواژه‌ها
Apoptosis؛ Endoplasmic reticulum- stress؛ Inflammation؛ Sciatic nerve؛ Sodium arsenite؛ Zingerone
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