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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
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CORM-2 Pretreatment Attenuates Inflammation-mediated Islet Dysfunction.

Xiang-Heng Cai1,2, Guan-Qiao Wang3,4, Rui Liang4,5

  • 1The First Central Clinical College, Tianjin Medical University, Tianjin, China.

Cell Transplantation
|May 5, 2020
PubMed
Summary
This summary is machine-generated.

Carbon monoxide-releasing molecule 2 (CORM-2) pretreatment reduces inflammation and apoptosis during human islet isolation. This improves islet viability, insulin secretion, and transplantation outcomes, offering a potential therapy for islet dysfunction.

Keywords:
CORM-2TNF-αinflammationislet functionislet transplantation

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Area of Science:

  • Islet biology and transplantation
  • Inflammation and immunology
  • Biomedical engineering

Background:

  • Human islet isolation involves stressful events that impair islet yield, viability, and function.
  • Proinflammatory cytokines and apoptosis are key mediators of islet dysfunction during isolation.
  • Carbon monoxide-releasing molecule 2 (CORM-2) is known for cytoprotective and anti-inflammatory effects, but its role in islet isolation is unexplored.

Purpose of the Study:

  • To investigate the effect of CORM-2 pretreatment on human islet isolation.
  • To evaluate CORM-2's impact on inflammation, apoptosis, viability, and function of isolated human islets.
  • To determine if CORM-2 can mitigate tumor necrosis factor-alpha (TNF-α)-induced islet dysfunction.

Main Methods:

  • Human islets were pretreated with CORM-2 prior to isolation.
  • Gene expression of inflammatory markers (e.g., tissue factor, ICAM-1, chemokines, TLR4, IL-1β, IL-6, TNF-α) was assessed.
  • Islet apoptosis rate, viability, and glucose-stimulated insulin secretion (GSIS) were measured.
  • Transplantation outcomes and TNF-α impairment effects were evaluated.

Main Results:

  • CORM-2 pretreatment significantly decreased the expression of key inflammatory genes.
  • Isolated islets from the CORM-2 group exhibited reduced apoptosis and improved viability.
  • Higher glucose-stimulated insulin secretion and functional gene expression were observed in CORM-2 pretreated islets.
  • CORM-2 pretreatment protected against TNF-α-induced impairment, improving GSIS and transplantation outcomes.

Conclusions:

  • CORM-2 demonstrates significant anti-inflammatory properties during human islet isolation.
  • CORM-2 pretreatment mitigates inflammation-mediated islet dysfunction ex vivo.
  • This approach holds promise for preserving long-term islet survival and function for transplantation.