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Mesenchymal stem cells inhibited the inflammation and oxidative stress in LPS-activated microglial cells through AMPK
Dayong Cao1, Haowen Qiao2, Dejiao He3
1Department of Burns, The First People's Hospital of Zhengzhou, Zhengzhou, 450000, Henan, People's Republic of China.
Abstract:
Microglia are the resident mononuclear immune cells of the central nervous system (CNS) and the activation of microglia contributes to the production of excessive neurotoxic factors. In particular, the overproduction of neurotoxic factors has critical effects on the development of brain injuries and neurodegenerative diseases. The human bone marrow-derived mesenchymal stem cells (hBM-MSCs) have blossomed into an effective approach with great potential for the treatment of neurodegenerative diseases and gliomas. The present study aimed to investigate the mechanism behind the therapeutic effect of hBM-MSCs on the activation of microglia in vitro. Specifically, the hBM-MSCs significantly inhibited the proliferation of lipopolysaccharide-activated microglial cells (LPS)-activated microglial cells. Additionally, we investigated whether the adenosine-monophosphate-activated protein kinase signaling (AMPK) pathway was involved in this process. Our data demonstrated that hBM-MSCs significantly increased the phosphorylated AMPK in LPS-activated microglial cells. In addition, our study indicated the inhibitory effect of hBM-MSCs on the pro-inflammatory mediators and oxidative stress by the AMPK pathway in LPS-activated microglial cells. These results could shed light on the understanding of the molecular basis for the inhibition of hBM-MSCs on LPS-activated microglial cells and provide a molecular mechanism for the hBM-MSCs implication in brain injuries and neurodegenerative diseases.
Insights
Human bone marrow-derived mesenchymal stem cells (hBM-MSCs) reduce the proliferation of activated microglial cells. This neuroprotective effect is mediated by the adenosine-monophosphate-activated protein kinase (AMPK) pathway, reducing inflammation and oxidative stress.
Area of Science:
- Neuroscience
- Immunology
- Stem Cell Biology
Background:
- Microglia, the central nervous system's immune cells, become overactivated, producing neurotoxic factors detrimental to brain health.
- This microglial overactivation is implicated in neurodegenerative diseases and brain injuries.
- Human bone marrow-derived mesenchymal stem cells (hBM-MSCs) show therapeutic promise for neurological conditions.
Purpose of the Study:
- To elucidate the mechanism by which hBM-MSCs exert therapeutic effects on activated microglia in vitro.
- To investigate the role of the adenosine-monophosphate-activated protein kinase (AMPK) signaling pathway in hBM-MSC-mediated microglial modulation.
Main Methods:
- In vitro study using lipopolysaccharide (LPS)-activated microglial cells.
- Treatment with hBM-MSCs.
- Assessment of microglial proliferation.
- Measurement of phosphorylated AMPK levels.
- Analysis of pro-inflammatory mediators and oxidative stress markers.
Main Results:
- hBM-MSCs significantly inhibited the proliferation of LPS-activated microglial cells.
- hBM-MSCs treatment led to increased phosphorylated AMPK in LPS-activated microglial cells.
- The AMPK pathway was identified as the mediator for hBM-MSC's inhibitory effects on pro-inflammatory mediators and oxidative stress.
Conclusions:
- hBM-MSCs effectively suppress microglial activation and proliferation.
- The therapeutic mechanism involves the activation of the AMPK pathway.
- These findings provide a molecular understanding of hBM-MSC's neuroprotective potential in brain injuries and neurodegenerative diseases.
