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Expression of death receptor apoptosis pathway- correlated factors in pancreatic tissue of mouse diabetic model

Authors :
MIAO Miao, LIU Yan, ZHANG Huan, ZHAO Huichao, LI Zhuofan, ZHANG Haolan, YUAN Panpan
Source :
Jichu yixue yu linchuang, Vol 43, Iss 8, Pp 1254-1258 (2023)
Publication Year :
2023
Publisher :
Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College., 2023.

Abstract

Objective To study the expression of apoptosis related factors in the apoptosis pathway of death receptor in the pancreas of mice diabetic models. Methods The mice were divided into control group and model group. They were injected alloxan intraperitoneally twice (120 mg/kg,80 mg/kg). Blood glucose was measured on the third and seventh days after the model was established; Pancreatic tissue was taken for HE observation, TUNEL was used to detect the apoptosis rate, and RT-qPCR was used to detect the mRNA expression of tumor necrosis factor receptor 1 (TNFR1), Fas-related death domain (FADD), caspase-8 and caspase-3. Results Compared with the control group, pancreatic acinar cells in the model group showed granular degeneration, capillary congestion, decreased islet volume and the number of cells in islets. Compared with the control group, the apoptosis rate of pancreatic cells in the model group was significantly increased (P<0.01). In addition, compared with the control group, the expression of Tnfr1, Fadd, caspase-8 and caspase-3 mRNA in the pancreas of the model group increased significantly or highly significantly on the third and seventh days (P<0.05 or P<0.01). Conclusions Alloxan could promote the over-expression of Tnfr1, Fadd, caspase-8 and caspase-3 mRNA in pancreatic tissue of diabetes model mice, and then induce apoptosis of pancreatic cells.

Details

Language :
Chinese
ISSN :
10016325
Volume :
43
Issue :
8
Database :
Directory of Open Access Journals
Journal :
Jichu yixue yu linchuang
Publication Type :
Academic Journal
Accession number :
edsdoj.9341b04f7c141988b2053a9e21da5b2
Document Type :
article
Full Text :
https://doi.org/10.16352/j.issn.1001-6325.2023.08.1254