The effects of tadalafil and pentoxifylline on apoptosis and nitric oxide synthase in liver ischemia/reperfusion injury

The aim of this study was to investigate the effects of tadalafil (TDF) and pentoxifylline (PTX) on hepatic apoptosis and the expressions of endothelial and inducible nitric oxide synthases (eNOS and iNOS) after liver ischemia/reperfusion (IR). Forty Wistar albino rats were randomly divided into five groups (n = 8) as follows: sham group; IR group with ischemia/reperfusion alone; low-dose and high-dose TDF groups received 2.5 mg/kg and 10 mg/kg TDF, respectively; and PTX group received 40 mg/kg PTX. Blood was collected for the analysis of serum alanine aminotransferase, aspartate aminotransferase, ?-glutamyl transferase, uric acid, malondialdehyde (MDA), and total antioxidant capacity (TAC). MDA and TAC also were measured in liver tissue. Histopathological examination was performed to assess the severity of hepatic injury. Apoptosis was evaluated using the apoptosis protease-activating factor 1 (APAF-1) antibody; the expressions of eNOS and iNOS were also assessed by immunohistochemistry in all groups. Serum alanine aminotransferase, aspartate aminotransferase, ?-glutamyl transferase, uric acid, MDA, and TAC, tissue MDA and TAC levels, hepatic injury, and score for extent and for intensity of eNOS, iNOS, and apoptosis protease-activating factor 1 were significantly different in TDF and PTX groups compared to the IR group. High dose-TDF and PTX have the best protective effect on IR-induced liver tissue damage. This study showed that TDF and PTX supplementation may be helpful in preventing free oxygen radical damage, lipid peroxidation, hepatocyte necrosis, and apoptosis in liver IR injury and minimizing liver damage. © 2016

Dergi Adı Kaohsiung Journal of Medical Sciences
Dergi Cilt Bilgisi 32
Dergi Sayısı 7
Sayfalar 339 - 347
Yayın Yılı 2016
Eser Adı
[dc.title]
The effects of tadalafil and pentoxifylline on apoptosis and nitric oxide synthase in liver ischemia/reperfusion injury
Yazar
[dc.contributor.author]
Bektaş, Sibel
Yazar
[dc.contributor.author]
Karakaya, Kemal
Yazar
[dc.contributor.author]
Can, Murat
Yazar
[dc.contributor.author]
Bahadır, Buarak
Yazar
[dc.contributor.author]
Güven, Berrak
Yazar
[dc.contributor.author]
Erdoğan, Nilsen
Yazar
[dc.contributor.author]
Özdamar, Şükrü Oğuz
Yayın Yılı
[dc.date.issued]
2016
Yayıncı
[dc.publisher]
Elsevier (Singapore) Pte Ltd
Yayın Türü
[dc.type]
article
Özet
[dc.description.abstract]
The aim of this study was to investigate the effects of tadalafil (TDF) and pentoxifylline (PTX) on hepatic apoptosis and the expressions of endothelial and inducible nitric oxide synthases (eNOS and iNOS) after liver ischemia/reperfusion (IR). Forty Wistar albino rats were randomly divided into five groups (n = 8) as follows: sham group; IR group with ischemia/reperfusion alone; low-dose and high-dose TDF groups received 2.5 mg/kg and 10 mg/kg TDF, respectively; and PTX group received 40 mg/kg PTX. Blood was collected for the analysis of serum alanine aminotransferase, aspartate aminotransferase, ?-glutamyl transferase, uric acid, malondialdehyde (MDA), and total antioxidant capacity (TAC). MDA and TAC also were measured in liver tissue. Histopathological examination was performed to assess the severity of hepatic injury. Apoptosis was evaluated using the apoptosis protease-activating factor 1 (APAF-1) antibody; the expressions of eNOS and iNOS were also assessed by immunohistochemistry in all groups. Serum alanine aminotransferase, aspartate aminotransferase, ?-glutamyl transferase, uric acid, MDA, and TAC, tissue MDA and TAC levels, hepatic injury, and score for extent and for intensity of eNOS, iNOS, and apoptosis protease-activating factor 1 were significantly different in TDF and PTX groups compared to the IR group. High dose-TDF and PTX have the best protective effect on IR-induced liver tissue damage. This study showed that TDF and PTX supplementation may be helpful in preventing free oxygen radical damage, lipid peroxidation, hepatocyte necrosis, and apoptosis in liver IR injury and minimizing liver damage. © 2016
Kayıt Giriş Tarihi
[dc.date.accessioned]
2019-12-23
Açık Erişim Tarihi
[dc.date.available]
2019-12-23
Yayın Dili
[dc.language.iso]
eng
Konu Başlıkları
[dc.subject]
Ischemia/reperfusion
Konu Başlıkları
[dc.subject]
Liver
Konu Başlıkları
[dc.subject]
Pentoxifylline
Konu Başlıkları
[dc.subject]
Tadalafil
Künye
[dc.identifier.citation]
Bektas, S., Karakaya, K., Can, M., Bahadir, B., Guven, B., Erdogan, N. ve Ozdamar, S. O. (2016). The effects of tadalafil and pentoxifylline on apoptosis and nitric oxide synthase in liver ischemia/reperfusion injury. The Kaohsiung Journal of Medical Sciences, 32(7), 339-347. doi:https://doi.org/10.1016/j.kjms.2016.05.005
Haklar
[dc.rights]
info:eu-repo/semantics/openAccess
ISSN
[dc.identifier.issn]
1607551X
İlk Sayfa Sayısı
[dc.identifier.startpage]
339
Son Sayfa Sayısı
[dc.identifier.endpage]
347
Dergi Adı
[dc.relation.journal]
Kaohsiung Journal of Medical Sciences
Dergi Sayısı
[dc.identifier.issue]
7
Dergi Cilt Bilgisi
[dc.identifier.volume]
32
Tek Biçim Adres
[dc.identifier.uri]
https://dx.doi.org/10.1016/j.kjms.2016.05.005
Tek Biçim Adres
[dc.identifier.uri]
https://hdl.handle.net/20.500.12628/8056
Tam Metin İndirmek için tıklayın Ön izleme
Görüntülenme Sayısı ( Şehir )
Görüntülenme Sayısı ( Ülke )
Görüntülenme Sayısı ( Zaman Dağılımı )
Görüntülenme
305
09.12.2022 tarihinden bu yana
İndirme
1
09.12.2022 tarihinden bu yana
Son Erişim Tarihi
28 Mayıs 2024 15:40
Google Kontrol
Tıklayınız
apoptosis aminotransferase groups damage injury hepatic tissue alanine aspartate transferase ?-glutamyl ischemia/reperfusion expressions factor protease-activating received (APAF-1) antibody evaluated Apoptosis assessed severity immunohistochemistry compared levels supplementation minimizing necrosis hepatocyte peroxidation radical oxygen preventing helpful showed
6698 sayılı Kişisel Verilerin Korunması Kanunu kapsamında yükümlülüklerimiz ve çerez politikamız hakkında bilgi sahibi olmak için alttaki bağlantıyı kullanabilirsiniz.

creativecommons
Bu site altında yer alan tüm kaynaklar Creative Commons Alıntı-GayriTicari-Türetilemez 4.0 Uluslararası Lisansı ile lisanslanmıştır.
Platforms