Mechanism of mouse bone marrow mesenchymal stem cells for alleviating kidney ischemic-reperfusion injury via glucose metabolism
10.3760/cma.j.cn421203-20210715-00194
- VernacularTitle:小鼠骨髓间充质干细胞通过糖代谢途径减轻肾缺血再灌注损伤
- Author:
Ruoyang CHEN
1
;
Dawei LI
;
Yao XU
;
Jiajin WU
;
Ming ZHANG
;
Xiaodong YUAN
Author Information
1. 上海交通大学医学院附属仁济医院泌尿外科 200120
- Keywords:
Kidney transplantation;
Ischemia-reperfusion injury;
Bone marrow stem cell
- From:
Chinese Journal of Organ Transplantation
2021;42(12):750-754
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the protective effects of exosomes derived from bone marrow mesenchymal stem cells(BMSC)on ischemia-reperfusion injury(IRI)in mice.Methods:A total of 30 C57BL/6 mice were randomly grouped into 6 groups of control, Norm-BMSC-exo, Hypo-BMSC-exo, IRI, Norm-BMSC-exo+ IRI and Hypo-BMSC-exo+ IRI.The model for IRI(25 min)was constructed.The serum levels of creatinine(Cr)and blood urea nitrogen(BUN)and histomorphology were examined at 24 h post-reperfusion.The levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β(IL-1β)monocyte chemoattractant protein-1(MCP-1)and interleukin-10 (IL-10)were measured.The survival rate was observed for 7 days post-IRI.We also detected macrophage polarization glycolysis and oxidative phosphorylation(OXPHOS).Results:Compared with IRI group, Norm-BMSC-exo+ IRI group showed low levels of creatinine(Cr)and blood urea nitrogen(BUN)and mild pathological injury.The protective effects were enhanced in Hypo-BMSC-exo+ IRI group.BMSC-exo pretreatment could significantly improve the survival rate of mice post-IRI.Reverse transcription-polymerase chain reaction(RT-PCR)revealed that BMSC-exo significantly lowered the levels of TNF-α, IL-1β, MCP-1 and elevated the level of IL-10.BMSC exosomes polarized macrophage toward an M2 phenotype.And Hypo-exo could reprogramme macrophages to undergo a metabolic switch toward OXPHOS and away from glycolysis.Conclusions:Hypo-BMSC-exo could improve kidney injury via inducing M2 polarization in macrophages through promoting OXPHOS and suppressing glycolysis.
