This is the authors' abstract. We don't add key points for this paper.
Hyperglycaemia-induced oxidative stress may disrupt insulin secretion and β-cell survival in diabetes mellitus by overproducing reactive oxygen species. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) exhibit antioxidant properties. However, the mechanisms by which hUC-MSCs protect β-cells from high glucose-induced oxidative stress remain underexplored. In this study, we showed that intravenously injected hUC-MSCs engrafted into the injured pancreas and promoted pancreatic β-cell function in a mouse model of type 1 diabetes mellitus. The in vitro study revealed that hUC-MSCs attenuated high glucose-induced oxidative stress and prevented β-cell impairment via the Nrf2/HO-1 signalling pathway. Nrf2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs, resulting in β-cell decompensation in a high-glucose environment. Overall, these findings provide novel insights into how hUC-MSCs protect β-cells from high glucose-induced oxidative stress.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: