Hyperglycaemia-induced oxidative stress may disrupt insulin secretion andβ-cell survival in diabetes mellitus by overproducing reactive oxygen species.Human umbilical cord-derived mesenchymal stem cells(hUC-MSCs)exhi...Hyperglycaemia-induced oxidative stress may disrupt insulin secretion andβ-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 protectβ-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 pancreaticβ-cell function in a mouse model of type 1 diabetes mellitus.The in vitro study revealed that hUC-MSCs attenuated high glucoseinduced oxidative stress and preventedβ-cell impairment via the Nrf2/HO-1 signalling pathway.Nrf2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs,resulting inβ-cell decompensation in a high-glucose environment.Overall,these findings provide novel insights into how hUC-MSCs protectβ-cells from high glucose-induced oxidative stress.展开更多
基金supported by grants from the National Natural Science Foundation of China(82070913)Shanghai Science and Technology Development Funds(20ZR1446000 and 22410713200)+1 种基金the Research Start-up Fund from Shanghai Fourth People’s Hospital(sykyqd01801)the Open Research Project of Shanghai Key Laboratory of Diabetes Mellitus(SHKLD-KF-2101).
文摘Hyperglycaemia-induced oxidative stress may disrupt insulin secretion andβ-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 protectβ-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 pancreaticβ-cell function in a mouse model of type 1 diabetes mellitus.The in vitro study revealed that hUC-MSCs attenuated high glucoseinduced oxidative stress and preventedβ-cell impairment via the Nrf2/HO-1 signalling pathway.Nrf2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs,resulting inβ-cell decompensation in a high-glucose environment.Overall,these findings provide novel insights into how hUC-MSCs protectβ-cells from high glucose-induced oxidative stress.
