CORM-2 Pretreatment Attenuates Inflammation-mediated Islet Dysfunction.
In this study, we found that CORM-2 pretreatment significantly decreased the expression of critical inflammatory genes, including tissue factor, intercellular adhesion molecule-1, chemokine (C-C motif) ligand 2, C-X-C motif chemokine 10, Toll-like receptor 4, interleukin-1β, interleukin-6, and tumor necrosis factor-α (TNF-α). The isolated islets of the CORM-2 pretreatment group showed reduced apoptotic rate, improved viability, and higher glucose-stimulated insulin secretion, and functional gene expression in comparison to control group. Importantly, CORM-2 pretreatment prevented the impairment caused by TNF-α, evidenced by the improved glucose-stimulated index and transplantation outcomes. The present study demonstrated the anti-inflammatory property of CORM-2 during human islet isolation, and we suggest that CORM-2 pretreatment is an appealing treatment to mitigate inflammation-mediated islet dysfunction during isolation and culture ex vivo and to preserve long-term islet survival and function.
PMID: 32364405 [PubMed - as supplied by publisher]
Source: Cell Transplantation - Category: Cytology Authors: Cai XH, Wang GQ, Liang R, Wang L, Liu TL, Zou JQ, Liu N, Liu Y, Wang SS, Shen ZY Tags: Cell Transplant Source Type: research