Investigating Oxidative Stress and Histopathological Changes in The Liver of Hyperglycemic Rats

Başak Işıldar; Meral Koyutürk

Makale detayları

Investigating Oxidative Stress and Histopathological Changes in The Liver of Hyperglycemic Rats

Yazarlar:

Başak Işıldar | Meral Koyutürk

Yayıncı:

Balıkesir University

Ana Başlıklar:

Sağlığın Geliştirilmesi | Veteriner Histoloji ve Embriyolojisi

Dergi:

Balıkesir Sağlık Bilimleri Dergisi Vol.14 Issue 1, pp.101-106

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001343774

pISSN:

2146-9601

Anahtar kelimeler:

Özet:

 Objective: This study aimed to investigate the impact of hyperglycemia on the liver in rats. Materials and Methods: An experimental diabetes was created by intraperitoneal streptozotocin administration to Sprague-Dawley rats, and blood glucose levels over 250 dlkg were counted as diabetic. The experiment was continued for 6 weeks, and weight and blood glucose were observed weekly. After sacrification, liver tissues were fixed with formaldehyde and enclosed in paraffin for histological analysis. Hematoxylin and eosin staining was carried out on 4 µm sections taken from paraffin blocks, and the sections were evaluated histopathologically. At the same time, apoptosis was examined immunohistochemically in those sections by active caspase-3 labeling. Finally, oxidative stress status in liver tissue was analyzed by hydrogen peroxide H2O2 and superoxide dismutase SOD levels. Results: The results revealed a significant elevation in H2O2 levels and a slight decline in SOD levels in the liver tissues in the hyperglycemia group. Additionally, apoptotic hepatocyte numbers were elevated. Histopathological analysis revealed disrupted lobular structure, dilatation of the central vein and sinusoids, hepatocyte shrinkage, and lymphocytic infiltration in the hyperglycemia group. Conclusion: This study underscores the critical role of apoptosis and oxidative stress in liver dysfunction caused by diabetes, highlighting the need for novel therapeutic strategies to protect against hyperglycemia-induced liver damage and improve outcomes for diabetic patients.

 Objective: This study aimed to investigate the impact of hyperglycemia on the liver in rats. Materials and Methods: An experimental diabetes was created by intraperitoneal streptozotocin administration to Sprague-Dawley rats, and blood glucose levels over 250 dlkg were counted as diabetic. The experiment was continued for 6 weeks, and weight and blood glucose were observed weekly. After sacrification, liver tissues were fixed with formaldehyde and enclosed in paraffin for histological analysis. Hematoxylin and eosin staining was carried out on 4 µm sections taken from paraffin blocks, and the sections were evaluated histopathologically. At the same time, apoptosis was examined immunohistochemically in those sections by active caspase-3 labeling. Finally, oxidative stress status in liver tissue was analyzed by hydrogen peroxide H2O2 and superoxide dismutase SOD levels. Results: The results revealed a significant elevation in H2O2 levels and a slight decline in SOD levels in the liver tissues in the hyperglycemia group. Additionally, apoptotic hepatocyte numbers were elevated. Histopathological analysis revealed disrupted lobular structure, dilatation of the central vein and sinusoids, hepatocyte shrinkage, and lymphocytic infiltration in the hyperglycemia group. Conclusion: This study underscores the critical role of apoptosis and oxidative stress in liver dysfunction caused by diabetes, highlighting the need for novel therapeutic strategies to protect against hyperglycemia-induced liver damage and improve outcomes for diabetic patients.

 Objective: This study aimed to investigate the impact of hyperglycemia on the liver in rats. Materials and Methods: An experimental diabetes was created by intraperitoneal streptozotocin administration to Sprague-Dawley rats, and blood glucose levels over 250 dlkg were counted as diabetic. The experiment was continued for 6 weeks, and weight and blood glucose were observed weekly. After sacrification, liver tissues were fixed with formaldehyde and enclosed in paraffin for histological analysis. Hematoxylin and eosin staining was carried out on 4 µm sections taken from paraffin blocks, and the sections were evaluated histopathologically. At the same time, apoptosis was examined immunohistochemically in those sections by active caspase-3 labeling. Finally, oxidative stress status in liver tissue was analyzed by hydrogen peroxide H2O2 and superoxide dismutase SOD levels. Results: The results revealed a significant elevation in H2O2 levels and a slight decline in SOD levels in the liver tissues in the hyperglycemia group. Additionally, apoptotic hepatocyte numbers were elevated. Histopathological analysis revealed disrupted lobular structure, dilatation of the central vein and sinusoids, hepatocyte shrinkage, and lymphocytic infiltration in the hyperglycemia group. Conclusion: This study underscores the critical role of apoptosis and oxidative stress in liver dysfunction caused by diabetes, highlighting the need for novel therapeutic strategies to protect against hyperglycemia-induced liver damage and improve outcomes for diabetic patients.

 Amaç: Bu çalışmada sıçanlarda hipergliseminin karaciğer üzerine etkisinin değerlendirilmesi amaçlandı. Gereç ve Yöntem: Sprague-Dawley tipi sıçanlarda, streptozotosin ile deneysel diyabet modeli oluşturuldu ve kan glikozunun 250 dlkgnin üzerinde olduğu sıçanlar diyabetik kabul edildi. 6 hafta süren deney boyunca, haftalık olarak kan glikozu ve ağırlık takibi yapıldı. Sakrifikasyondan sonra alınan karaciğer dokuları, histolojik incelemeler için formaldehit ile fikse edildi ve doku takibinin ardından parafine gömülmüştür. Parafin bloklardan alınan 4 umlik kesitlerde hematoksilen ve eozin boyaması yapıldı ve kesitler histopatolojik olarak değerlendirildi. Aynı zamanda bu kesitlerde aktif kazpaz-3 işaretlemesi ile apoptoz, immünohistokimyasal olarak incelendi. Son olarak karaciğer dokusundaki oksidatif stres durumu, hidrojen peroksit H2O2 ve süperoksit dismutaz SOD seviyeleri üzerinden analiz edildi. Bulgular: Sonuçlara göre, hiperglisemi grubundaki sıçanlara ait karaciğerlerde H2O2 düzeyinin anlamlı derecede yükseldiği ve SOD düzeyinin bir miktar düştüğü, hepatositlerde apoptoza giden hücre sayısının arttığı görüldü. Karaciğer histopatolojisi, hiperglisemi grubunda bozulmuş karaciğer lobüler yapısını, santral ven ve sinusoidal dilatasyonları, hepatositlerde küçülmeyi ve lenfositik infiltrasyonu ortaya koydu. Sonuç: Bu çalışma, diyabet kaynaklı karaciğer fonksiyon bozukluğunda oksidatif stres ve apoptozun kritik rolünü vurgulayarak, hiperglisemi kaynaklı karaciğer hasarına karşı koruma sağlamak ve diyabetli hastalarda sonuçları iyileştirmek için yeni tedavi stratejilerine olan ihtiyacı vurgulamaktadır.

Makale detayları

Investigating Oxidative Stress and Histopathological Changes in The Liver of Hyperglycemic Rats

Yazarlar:

Başak Işıldar | Meral Koyutürk

Yayıncı:

Balıkesir University

Ana Başlıklar:

Sağlığın Geliştirilmesi | Veteriner Histoloji ve Embriyolojisi

Dergi:

Balıkesir Sağlık Bilimleri Dergisi Vol.14 Issue 1, pp.101-106

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001343774

pISSN:

2146-9601

Experimental Diabetes

Liver

Oxidative Stress

Histopathology

Apoptosis.Deneysel Diyabet

Karaciğer

Oksidatif Stres

Histopatoloji

Apoptoz.

Sayı

Makale detayları

Yazarlar: Başak Işıldar | Meral Koyutürk

Yayıncı: Balıkesir University

Ana Başlıklar: Sağlığın Geliştirilmesi | Veteriner Histoloji ve Embriyolojisi

Dergi: Balıkesir Sağlık Bilimleri Dergisi Vol.14 Issue 1, pp.101-106

Belge Tipi: Makale

Yayın Tarihi: 3/2025

Belge Dili: İngilizce

Document ID (Org No.): 2001343774

pISSN: 2146-9601

Sayı

Yazarlar:

Başak Işıldar | Meral Koyutürk

Yayıncı:

Balıkesir University

Ana Başlıklar:

Sağlığın Geliştirilmesi | Veteriner Histoloji ve Embriyolojisi

Dergi:

Balıkesir Sağlık Bilimleri Dergisi Vol.14 Issue 1, pp.101-106

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001343774

pISSN:

2146-9601