The effect of N-acetyl cysteine on H2O2 mediated oxidative stress in Whartonʼs jelly derived mesenchymal stem cells
Background: Hypoxic stress is a crucial factor for retaining the cell survival in injured tissue. Overcoming this issue is the key for successful cellular regenerative therapy. Therefore the purpose of this study was to investigate whether the in-vitro pretreatment of Whartonʼs Jelly (WJ) derived Me...
Main Authors: | , , , |
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Format: | Article |
Language: | English |
Published: |
University of the Punjab
2017-08-01
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Series: | Advancements in Life Sciences |
Subjects: | |
Online Access: | http://www.als-journal.com/445-17/ |
Summary: | Background: Hypoxic stress is a crucial factor for retaining the cell survival in injured tissue. Overcoming this issue is the key for successful cellular regenerative therapy. Therefore the purpose of this study was to investigate whether the in-vitro pretreatment of Whartonʼs Jelly (WJ) derived Mesenchymal stem cells (WJ-MSCs) with an antioxidant, namely N-acetylcysteine (NAC), can improve the efficacy of WJ-MSCs for transplantation purpose.
Methods: WJ-MSCs were cultured with or without NAC at different concentrations (0.1mM, 1mM and 10mM). To simulate oxidative stress conditions, cultures were exposed to hydrogen peroxide (H2O2) 100 µM for 1 hour. Cytoprotective effect of NAC was evaluated by determining cell injury, viability, and proliferation. The oxidative stress is assessed by measuring the activity of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malodialdehyde (MDA).
Results: Pretreatment of WJ-MSCs with NAC increased their viability and proliferation in concentration-dependent manner. Furthermore, 10 mM NAC significantly reduced the H2O2 induced oxidative stress by enhancing the activity of GSH, SOD, and CAT and reduced the level of MDA
Conclusion: The study results indicate that NAC may abrogate H2O2 induced oxidative-stress of WJ-MSCs. This study provides basis to explore NAC effect on WJ-MSCs survival without cytotoxicity. |
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ISSN: | 2310-5380 2310-5380 |