Human umbilical cord-derived mesenchymal stem cells alleviate oxidative stress-induced islet impairment via the Nrf2/HO-1 axis
作者机构:Shanghai Diabetes InstituteDepartment of Endocrinology and MetabolismShanghai Key Laboratory of Diabetes MellitusShanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200233China Department of Endocrinology&MetabolismShanghai Fourth People’s HospitalSchool of MedicineTongji UniversityShanghai 200434China Translational Medical Center for Stem Cell TherapyShanghai East HospitalSchool of MedicineTongji UniversityShanghai 200092China Stem Cell Translational Research CenterTongji HospitalSchool of MedicineTongji UniversityShanghai 200065China
出 版 物:《Journal of Molecular Cell Biology》 (分子细胞生物学报(英文版))
年 卷 期:2023年第15卷第5期
页 面:38-51页
核心收录:
学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金:supported by grants from the National Natural Science Foundation of China(82070913) Shanghai Science and Technology Development Funds(20ZR1446000 and 22410713200) 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)
主 题:type 1 diabetes β-cell protection mesenchymal stem cells oxidative stress Nrf2
摘 要:Hyperglycaemia-induced oxidative stress may disrupt insulin secretion andβ-cell survival in diabetes mellitus by overproducing reactive oxygen *** umbilical cord-derived mesenchymal stem cells(hUC-MSCs)exhibit antioxidant ***,the mechanisms by which hUC-MSCs protectβ-cells from high glucose-induced oxidative stress remain *** 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 *** in vitro study revealed that hUC-MSCs attenuated high glucoseinduced oxidative stress and preventedβ-cell impairment via the Nrf2/HO-1 signalling ***2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs,resulting inβ-cell decompensation in a high-glucose ***,these findings provide novel insights into how hUC-MSCs protectβ-cells from high glucose-induced oxidative stress.