Dergiler / Turkish Journal of Veterinary and Animal Sciences / 2014 / Cilt: 38 - Sayı: 4

Immunohistochemical localization of glutathione peroxidase 1 enzyme and its gene expression by RT-PCR in the liver tissue of healthy and diabetic mice

Sayfa
363–369
Yayın Tarihi
2014-04-01
DOI
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

In conclusion, diabetes mellitus causes a decrease in the level of GPx1 activity, which is known to be one of the antioxidant enzymes.

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Amaç & Hipotez:The purpose of this study is to examine the gene expression level of glutathione peroxidase 1 (GPx1) in the liver of healthy and diabetic mice, its localization in the tissue, and structural changes in the liver.
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Temel Bulgular & Veri:In this study, 36 Swiss albino mice were divided into 3 groups: experimental (diabetic) (n = 15), sham (n = 15), and control (n = 6).
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Sonuç & Katkı:In conclusion, diabetes mellitus causes a decrease in the level of GPx1 activity, which is known to be one of the antioxidant enzymes.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Diabetes mellitus · liver · GPx1

Özet

The purpose of this study is to examine the gene expression level of glutathione peroxidase 1 (GPx1) in the liver of healthy and diabetic mice, its localization in the tissue, and structural changes in the liver. In this study, 36 Swiss albino mice were divided into 3 groups: experimental (diabetic) (n = 15), sham (n = 15), and control (n = 6). Streptozotocin (100 mg/kg) was intraperitoneally administered to mice in the experimental group. While the gene expression level of GPx1 was determined using the RT-PCR method, its localization in the liver was determined using an immunohistochemical method. The GPx1 enzyme activity of the experimental group was lower compared to the sham and control groups (P < 0.05). There was no difference between the experimental and sham groups in terms of the gene expression of GPx1; however, a statistically insignificant decrease was observed in the experimental group compared to the sham group. GPx1 had similar immunolocalization in all groups, but GPx1 immunoreactivity was lower in the experimental group compared to the other groups. Enlargement of hepatocytes and their nuclei as well as the presence of intranuclear inclusion bodies were observed in the experimental group. In conclusion, diabetes mellitus causes a decrease in the level of GPx1 activity, which is known to be one of the antioxidant enzymes.

Abstract

The purpose of this study is to examine the gene expression level of glutathione peroxidase 1 (GPx1) in the liver of healthy and diabetic mice, its localization in the tissue, and structural changes in the liver. In this study, 36 Swiss albino mice were divided into 3 groups: experimental (diabetic) (n = 15), sham (n = 15), and control (n = 6). Streptozotocin (100 mg/kg) was intraperitoneally administered to mice in the experimental group. While the gene expression level of GPx1 was determined using the RT-PCR method, its localization in the liver was determined using an immunohistochemical method. The GPx1 enzyme activity of the experimental group was lower compared to the sham and control groups (P < 0.05). There was no difference between the experimental and sham groups in terms of the gene expression of GPx1; however, a statistically insignificant decrease was observed in the experimental group compared to the sham group. GPx1 had similar immunolocalization in all groups, but GPx1 immunoreactivity was lower in the experimental group compared to the other groups. Enlargement of hepatocytes and their nuclei as well as the presence of intranuclear inclusion bodies were observed in the experimental group. In conclusion, diabetes mellitus causes a decrease in the level of GPx1 activity, which is known to be one of the antioxidant enzymes.

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Bu Makaleye Atıf Yap

DEPREM, T., GÜLMEZ, N. (2014). Immunohistochemical localization of glutathione peroxidase 1 enzyme and its gene expression by RT-PCR in the liver tissue of healthy and diabetic mice. Turkish Journal of Veterinary and Animal Sciences, Cilt: 38 - Sayı: 4, 363–369. https://ajindex.com/articles/121547

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Kaynakça (9)

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