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Updated: Mar 26, 2026
Isolated Pancreatic Islet Treatment and Apoptosis Measurement
Published on: May 2, 2025
Effect of CXCL10 receptor antagonist on islet cell apoptosis in a type I diabetes rat model
Jinshui He1, Chaowei Lian1, Yanling Fang1
1Department of Pediatrics, Zhangzhou Hospital Affiliated to Fujian Medical University Zhangzhou 363000, Fujian, P. R. China.
Abstract:
In recent years, the incidence of type 1 diabetes mellitus (T1DM) has been increasing. The role of CXCL10 and its receptor, CXCR3, in the occurrence of T1DM has drawn lots of research interests, as the disease incidence was correlated with their expression levels. We thus used an antagonist of CXCR3, NBI-74330, to block the specific binding, for further observation of islet cell apoptosis in a T1MD rat model. A total of 80 SD rats were given STZ intraperitoneally for generating T1DM model. Different concentrations of NBI-74330 were then applied, followed by the collection of blood and pancreatic tissue samples. CXCL10 and CXCR3 levels were detected by enzyme linked immunosorbent assay (ELISA), followed by expressional assays in pancreatic tissues by real-time PCR, Western blotting and flow cytometry. Compared to control group, model rats had significantly elevated blood glucose level (>16.7 mmol/L), with depressed CXCL10 and CXCR3 levels compared to model group (P<0.05). After NBI-74330 treatment, mRNA and protein levels of CXCL10 and CXCR3 were significantly lowered, with significantly decreased apoptotic cell ratios compared to model group (P<0.05). CXCL10 receptor antagonist NBI-74330 can inhibit the apoptosis of pancreatic islet cells in T1DM rats.
Insights
CXCL10 receptor antagonist NBI-74330 reduces pancreatic islet cell apoptosis in a type 1 diabetes rat model. This finding offers a potential therapeutic strategy for type 1 diabetes mellitus (T1DM).
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Type 1 diabetes mellitus (T1DM) incidence is rising globally.
- CXCL10 and its receptor CXCR3 are implicated in T1DM pathogenesis.
- Understanding the role of CXCL10/CXCR3 signaling in T1DM is crucial.
Purpose of the Study:
- To investigate the therapeutic potential of a CXCR3 antagonist, NBI-74330, in a T1DM rat model.
- To evaluate the effect of NBI-74330 on pancreatic islet cell apoptosis.
- To analyze the modulation of CXCL10 and CXCR3 expression by NBI-74330.
Main Methods:
- Streptozotocin (STZ) induced T1DM in 80 Sprague-Dawley rats.
- Administration of varying concentrations of CXCR3 antagonist NBI-74330.
- Measurement of blood glucose, CXCL10, and CXCR3 levels via ELISA.
- Assessment of gene and protein expression using real-time PCR, Western blotting, and flow cytometry.
Main Results:
- STZ-induced rats exhibited hyperglycemia (>16.7 mmol/L) and altered CXCL10/CXCR3 levels.
- NBI-74330 treatment significantly reduced mRNA and protein levels of CXCL10 and CXCR3.
- A significant decrease in pancreatic islet cell apoptosis was observed post-NBI-74330 treatment.
Conclusions:
- CXCL10 receptor antagonist NBI-74330 effectively inhibits pancreatic islet cell apoptosis in a T1DM rat model.
- Targeting the CXCL10/CXCR3 pathway presents a promising therapeutic avenue for T1DM.
- Further research is warranted to explore NBI-74330's clinical applicability in T1DM management.
