Jujuboside A inhibits oxidative stress damage and enhances immunomodulatory capacity of human umbilical cord mesenchymal stem cells through up-regulating IDO expression.
10.1016/S1875-5364(22)60176-6
- Author:
Ji-Cong CHEN
1
;
Hong-He XIAO
1
;
Qiang ZHANG
1
;
Liang KONG
1
;
Tian-Min WANG
1
;
Yu TIAN
1
;
Yu-Meng ZHAO
1
;
He LI
1
;
Jin-Ming TIAN
1
;
Cui WANG
2
;
Jing-Xian YANG
3
Author Information
1. School of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, China.
2. Department of Neurology, Dalian Municipal Central Hospital Affiliated to Dalian Medical University, Dalian 116033, China. Electronic address: wangc817@163.com.
3. School of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, China. Electronic address: jingxianyang63@126.com.
- Publication Type:Journal Article
- Keywords:
Human umbilical cord mesenchymal stem cells;
Immunomodulation;
Indoleamine 2,3-dioxygenase;
Jujuboside A;
Oxidative stress
- MeSH:
Animals;
Cell Differentiation;
Humans;
Hydrogen Peroxide/metabolism*;
Mesenchymal Stem Cells;
Oxidative Stress;
Rats;
Saponins;
Umbilical Cord/metabolism*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2022;20(7):494-505
- CountryChina
- Language:English
-
Abstract:
Impaired immunomodulatory capacity and oxidative stress are the key factors limiting the effectiveness of mesenchymal stem cell transplantation therapy. The present study was aimed to investigate the effects of jujuboside A (JuA) on the protective effect and immunomodulatory capacity of human umbilical cord mesenchymal stem cells (hUC-MSCs). Hydrogen peroxide was used to establish an oxidative damage model of hUC-MSCs, while PBMCs isolated from rats were used to evaluate the effect of JuA pre-treatment on the immunomodulatory capacity of hUC-MSCs. Furthermore, Hoechst 33258 staining, lactate dehydrogenase test, measurement of malondialdehyde, Western blot, high-performance liquid chromatography; and flow cytometry were performed. Our results indicated that JuA (25 μmol·L-1) promoted the proliferation of hUC-MSCs, but did not affect the differentiating capability of these cells. JuA pre-treatment inhibited apoptosis, prevented oxidative damage, and up-regulated the protein expression of nuclear factor-erythroid factor 2-related factor 2 and heme oxygenase 1 in hUC-MSCs in which oxidative stress was induced with H2O2. In addition, JuA pre-treatment enhanced the inhibitory effect of hUC-MSCs against abnormally activated PBMCs, which was related to stimulation of the expression and activity of indoleamine 2,3-dioxygenase. In conclusion, our results demonstrate that JuA pre-treatment can enhance the survival and immunomodulatory ability through pathways related to oxidative stress, providing a new option for the improvement of hUC-MSCs in the clinical setting.
