Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma
Aim: Cigarette smoking is a common addictive manner and one of the greatest threats to health. Nicotine is one of the main components of cigarette. The aim of this study was to reveal the effect of cotinine which is an active metabolite of nicotine, on peripheral nerve injury in rats. Material and M...
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Format: | Article |
Language: | English |
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Duzce University
2021-08-01
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Series: | Düzce Tıp Fakültesi Dergisi |
Subjects: | |
Online Access: | https://dergipark.org.tr/tr/download/article-file/1623328 |
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author | Rıfat Akdağ Gülnur Take Emin Çağıl Ali Dalgıç Uğur Soylu |
author_facet | Rıfat Akdağ Gülnur Take Emin Çağıl Ali Dalgıç Uğur Soylu |
author_sort | Rıfat Akdağ |
collection | DOAJ |
description | Aim: Cigarette smoking is a common addictive manner and one of the greatest threats to health. Nicotine is one of the main components of cigarette. The aim of this study was to reveal the effect of cotinine which is an active metabolite of nicotine, on peripheral nerve injury in rats.
Material and Methods: We studied 42 male adult albino-Wistar rats that were divided into three groups with simple randomization method. Group 1 were given Cotinine® (C-5923-sigma) intraperitoneally, at a dose of 0.3 mg/kg/day for 21 days. Group 2 were given ethyl alcohol, the solvent of Cotinine in the same way, dose and period. Group 3 were subjected to sciatic nerve compression injury by a clip, which has a closing pressure of 50 gr/cm2. Group 1 and 2 were subjected to the same type of injury at the end of 21 days. Four weeks later after trauma, both three groups were sacrificed and injured sciatic nerve sections are taken for histopathological analysis.
Results: It was observed that cotinine aggravated the traumatic degeneration and as privileged caused to fibrosis. In the Schwann cells of thick-myelinated fibers exhibited higher grades of degeneration and mitochondrial augmentation. According to the multiple comparison results, the number of Wallerian degenerations in the trauma group was significantly lower than in both the drug-control (p=0.016) and drug (p<0.001) groups. This situation was estimated as a response to oxidative stress.
Conclusion: This study reveals that peripheral nerve regeneration after traumatic injury may be affected negatively in smokers. |
first_indexed | 2024-03-11T20:35:37Z |
format | Article |
id | doaj.art-bf87f2b038974421848418caa4814531 |
institution | Directory Open Access Journal |
issn | 1307-671X |
language | English |
last_indexed | 2024-03-11T20:35:37Z |
publishDate | 2021-08-01 |
publisher | Duzce University |
record_format | Article |
series | Düzce Tıp Fakültesi Dergisi |
spelling | doaj.art-bf87f2b038974421848418caa48145312023-10-02T07:07:18ZengDuzce UniversityDüzce Tıp Fakültesi Dergisi1307-671X2021-08-0123215716310.18678/dtfd.89265497Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir ÇalışmaRıfat Akdağ0Gülnur Take1Emin Çağıl2Ali Dalgıç3Uğur Soylu4SBÜ Bursa Yüksek İhtisas Eğitim Araştırma Hastanesi Beyin ve Sinir Cerrahi KliniğiGazi Üniversitesi Tıp Fakültesi Histoloji Ve Embriyoloji ABDAnkara Şehir Hastanesi Beyin ve Sinir Cerrahisi KliniğiAnkara Şehir Hastanesi Beyin ve Sinir Cerrahisi KliniğiSBÜ Bursa Yüksek İhtisas Eğitim Araştırma Hastanesi Beyin ve Sinir Cerrahi KliniğiAim: Cigarette smoking is a common addictive manner and one of the greatest threats to health. Nicotine is one of the main components of cigarette. The aim of this study was to reveal the effect of cotinine which is an active metabolite of nicotine, on peripheral nerve injury in rats. Material and Methods: We studied 42 male adult albino-Wistar rats that were divided into three groups with simple randomization method. Group 1 were given Cotinine® (C-5923-sigma) intraperitoneally, at a dose of 0.3 mg/kg/day for 21 days. Group 2 were given ethyl alcohol, the solvent of Cotinine in the same way, dose and period. Group 3 were subjected to sciatic nerve compression injury by a clip, which has a closing pressure of 50 gr/cm2. Group 1 and 2 were subjected to the same type of injury at the end of 21 days. Four weeks later after trauma, both three groups were sacrificed and injured sciatic nerve sections are taken for histopathological analysis. Results: It was observed that cotinine aggravated the traumatic degeneration and as privileged caused to fibrosis. In the Schwann cells of thick-myelinated fibers exhibited higher grades of degeneration and mitochondrial augmentation. According to the multiple comparison results, the number of Wallerian degenerations in the trauma group was significantly lower than in both the drug-control (p=0.016) and drug (p<0.001) groups. This situation was estimated as a response to oxidative stress. Conclusion: This study reveals that peripheral nerve regeneration after traumatic injury may be affected negatively in smokers.https://dergipark.org.tr/tr/download/article-file/1623328sigaranikotinkotininperiferik sinirtravmacigarettenikotinecotinineperipheral nervetrauma |
spellingShingle | Rıfat Akdağ Gülnur Take Emin Çağıl Ali Dalgıç Uğur Soylu Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma Düzce Tıp Fakültesi Dergisi sigara nikotin kotinin periferik sinir travma cigarette nikotine cotinine peripheral nerve trauma |
title | Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma |
title_full | Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma |
title_fullStr | Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma |
title_full_unstemmed | Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma |
title_short | Periferik Sinir Yaralanmalarında Kotinin Etkileri: Deneysel Bir Çalışma |
title_sort | periferik sinir yaralanmalarinda kotinin etkileri deneysel bir calisma |
topic | sigara nikotin kotinin periferik sinir travma cigarette nikotine cotinine peripheral nerve trauma |
url | https://dergipark.org.tr/tr/download/article-file/1623328 |
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