Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model

In order to study the protection mechanism of liraglutide on the infectious lesion of the retina of type I diabetes, in this experiment, a mouse model of type I diabetes was established by induction with streptozotocin (STZ) and feeding with high-fat and high-sugar diet. After observing the living c...

Full description

Bibliographic Details
Main Authors: Lingling Wu, Lijuan Gao, Yaohui Cao, Fengju Chen, Ting Sun, Yahong Liu
Format: Article
Language:English
Published: Elsevier 2019-12-01
Series:Saudi Journal of Biological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1319562X19301949
id doaj-d34d4524f52347dd8c60f1cfce039149
record_format Article
spelling doaj-d34d4524f52347dd8c60f1cfce0391492020-11-25T02:07:55ZengElsevierSaudi Journal of Biological Sciences1319-562X2019-12-0126820962101Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse modelLingling Wu0Lijuan Gao1Yaohui Cao2Fengju Chen3Ting Sun4Yahong Liu5Department of Gynaecology, Second Affiliated Hospital of Xingtai Medical College, Xingtai City 054000, ChinaDepartment of Clinical Medicine, Xingtai Medical College, Xingtai City 054000, ChinaDepartment of Gynaecology, Second Affiliated Hospital of Xingtai Medical College, Xingtai City 054000, China; Corresponding author.Release Therapy Division, Second Affiliated Hospital of Xingtai Medical College, Xingtai City 054000, ChinaDepartment of Gynaecology, Second Affiliated Hospital of Xingtai Medical College, Xingtai City 054000, ChinaDepartment of Endocrinology, Second Affiliated Hospital of Xingtai Medical College, Xingtai City 054000, ChinaIn order to study the protection mechanism of liraglutide on the infectious lesion of the retina of type I diabetes, in this experiment, a mouse model of type I diabetes was established by induction with streptozotocin (STZ) and feeding with high-fat and high-sugar diet. After observing the living conditions of the modeled mice and detecting their fasting blood glucose (FBG), it was found that the modeled mice exhibited clinically similar symptoms in patients with type I diabetes, and their FBG was larger than 16.7 mmol/L, indicating that the experimental mouse model was obtained. The mice were divided into groups. The control group was divided into negative control group (A), light positive control group (B), diabetic control group (C), and diabetes care group (D) according to different treatment methods, and the experimental group was divided into treatment group 1 (LR1), treatment group 2 (LR2) and treatment group 3 (LR3) according to different injection doses. The eyes of mice in each group were extracted and retinal tissue sections were made, and the sections were stained with HE. The retinal morphology was observed and it was found that compared with group A, the outer nucleus layer was significantly thinner in group B and C, and the group D was the thinnest. After treatment with liraglutide, the outer nuclear layer of LR1 group and LR2 group LR3 group recovered significantly, indicating that liraglutide had protective effect on type I diabetes and light-induced damage of mouse retinal photoreceptor cells. Immunohistochemistry was used to detect p-Erk1/2 and ASK1 protein contents in retina. It was found that compared with the negative control group and the light control group, p-Erk1/2 protein contents in LR1, LR2 and LR3 groups were significantly increased, showing statistical significance. Compared with the negative control group and the light control group, ASK1 protein content in LR1, LR2 and LR3 groups significantly decreased. This suggested that the protective mechanism of liraglutide on retinopathy was related to up-regulation of antioxidant protein p-Erk1/2 and down-regulation of apoptosis-related protein ASK1, that is to say, the action site of liraglutide may be related to this. Through real-time quantitative detection of the Trx gene expression level in diabetic and photodamaged mice, it was found that compared with the diabetic light group, the Trx expression level in mice treated with liraglutide showed a significant up-regulated trend, suggesting that the protective mechanism of liraglutide on retinopathy was related to the up-regulated expression of antioxidant protein Trx. Therefore, liraglutide has a certain protective effect on diabetic retinal injury, and its mechanism is related to the up-regulation of p-Erk1/2 and Trx antioxidant protein, and the down-regulation of apoptosis-related protein ASK1. Keywords: Diabetic retinopathy, Diabetes, Liraglutide, Retina, Mousehttp://www.sciencedirect.com/science/article/pii/S1319562X19301949
collection DOAJ
language English
format Article
sources DOAJ
author Lingling Wu
Lijuan Gao
Yaohui Cao
Fengju Chen
Ting Sun
Yahong Liu
spellingShingle Lingling Wu
Lijuan Gao
Yaohui Cao
Fengju Chen
Ting Sun
Yahong Liu
Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
Saudi Journal of Biological Sciences
author_facet Lingling Wu
Lijuan Gao
Yaohui Cao
Fengju Chen
Ting Sun
Yahong Liu
author_sort Lingling Wu
title Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
title_short Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
title_full Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
title_fullStr Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
title_full_unstemmed Analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
title_sort analysis of the protective mechanism of liraglutide on retinopathy based on diabetic mouse model
publisher Elsevier
series Saudi Journal of Biological Sciences
issn 1319-562X
publishDate 2019-12-01
description In order to study the protection mechanism of liraglutide on the infectious lesion of the retina of type I diabetes, in this experiment, a mouse model of type I diabetes was established by induction with streptozotocin (STZ) and feeding with high-fat and high-sugar diet. After observing the living conditions of the modeled mice and detecting their fasting blood glucose (FBG), it was found that the modeled mice exhibited clinically similar symptoms in patients with type I diabetes, and their FBG was larger than 16.7 mmol/L, indicating that the experimental mouse model was obtained. The mice were divided into groups. The control group was divided into negative control group (A), light positive control group (B), diabetic control group (C), and diabetes care group (D) according to different treatment methods, and the experimental group was divided into treatment group 1 (LR1), treatment group 2 (LR2) and treatment group 3 (LR3) according to different injection doses. The eyes of mice in each group were extracted and retinal tissue sections were made, and the sections were stained with HE. The retinal morphology was observed and it was found that compared with group A, the outer nucleus layer was significantly thinner in group B and C, and the group D was the thinnest. After treatment with liraglutide, the outer nuclear layer of LR1 group and LR2 group LR3 group recovered significantly, indicating that liraglutide had protective effect on type I diabetes and light-induced damage of mouse retinal photoreceptor cells. Immunohistochemistry was used to detect p-Erk1/2 and ASK1 protein contents in retina. It was found that compared with the negative control group and the light control group, p-Erk1/2 protein contents in LR1, LR2 and LR3 groups were significantly increased, showing statistical significance. Compared with the negative control group and the light control group, ASK1 protein content in LR1, LR2 and LR3 groups significantly decreased. This suggested that the protective mechanism of liraglutide on retinopathy was related to up-regulation of antioxidant protein p-Erk1/2 and down-regulation of apoptosis-related protein ASK1, that is to say, the action site of liraglutide may be related to this. Through real-time quantitative detection of the Trx gene expression level in diabetic and photodamaged mice, it was found that compared with the diabetic light group, the Trx expression level in mice treated with liraglutide showed a significant up-regulated trend, suggesting that the protective mechanism of liraglutide on retinopathy was related to the up-regulated expression of antioxidant protein Trx. Therefore, liraglutide has a certain protective effect on diabetic retinal injury, and its mechanism is related to the up-regulation of p-Erk1/2 and Trx antioxidant protein, and the down-regulation of apoptosis-related protein ASK1. Keywords: Diabetic retinopathy, Diabetes, Liraglutide, Retina, Mouse
url http://www.sciencedirect.com/science/article/pii/S1319562X19301949
work_keys_str_mv AT linglingwu analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
AT lijuangao analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
AT yaohuicao analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
AT fengjuchen analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
AT tingsun analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
AT yahongliu analysisoftheprotectivemechanismofliraglutideonretinopathybasedondiabeticmousemodel
_version_ 1724928887567155200