Repair mechanism of human umbilical cord mesenchymal stem cell-derived exosome on neuronal ischemia and hypoxia injury
10.3760/cma.j.issn.1671-0282.2020.07.008
- VernacularTitle:人脐带间充质干细胞来源的外泌体对神经细胞缺血缺氧损伤修复机制研究
- Author:
Changlong HU
1
;
Wenqin ZHOU
;
Lu GE
;
Yongzhong FAN
;
Peng WANG
Author Information
1. 江苏省丹阳市人民医院神经外科 212300
- From:
Chinese Journal of Emergency Medicine
2020;29(7):934-940
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of human umbilical cord mesenchymal stem cell-derived exosome (hucMSC-ex) on proliferation, migration, apoptosis and autophagy in ischemia-anoxia neurons, and to provide a theoretical study for clinical research on stroke.Methods:Primary glial cells were cultured and OGD model was established. Then, these cells were incubated with huMSC-exosome. The inhibition rate of proliferation was detected by MTT assay. Apoptosis was observed by flow cytometry. The expressions of apoptosis related proteins were confirmed by RT-PCR and Western blot. The expressions of autophagy related proteins and PI3K/Akt signal were observed by Western blot. The data were analyzed using SPSS 17.0 software, multiple-group comparisons were performed using one-way ANOVA, and SNK- q test was used for pairwise comparison between groups. Results:MTT assay showed that OGD could inhibit cell proliferation of primary glial cells. After incubation with hucMSC-ex for 2 h, the inhibition rate of cell proliferation was lower than that of the control. The flow cytometry technology showed that hucMSC-ex reduced cell apoptosis. The cell migration experiments showed that OGD reduced cell migration capacity, but cell migration increased after exosomal incubation. RT-PCT and Western blot showed that OGD induced autophagy and apoptosis, hucMSC-ex activated PI3K/Akt signaling pathway, inhibited the expression of Bax and Caspase-3 (both P<0.05), and promoted the expression of Bcl-2 ( P<0.05). hucMSC-ex inhibited the expression of Beclin-1, Atg3 and LC3-Ⅱ(al l P<0.01). Conclusions:huMSC-exosome promote the proliferation and migration in ischemia-anoxia-injured neurons and inhibit the apoptosis and autophagy. The mechanism that hucMSC-ex repaired the injured nerve cells might be associated with PI3K/Akt signaling pathway.
