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Assessing Neuroprotective Effects of Glycyrrhizae Radix et Rhizoma Extract Using a Transient Middle Cerebral Artery Occlusion Mouse Model
Published on: December 9, 2018
Ginsenoside Rg1 attenuates cerebral ischemia-reperfusion injury through inhibiting the inflammatory activation of
Yue Guan1, Yan-Li Cao2, Jia-Wei Liu2
1Department of Clinical Medicine, Heilongjiang Nursing College, Harbin, 150001, Heilongjiang Province, China.
Abstract:
It is recognized that the cerebral ischemia/reperfusion (I/R) injury triggers inflammatory activation of microglia and supports microglia-driven neuronal damage. Our previous studies have shown that ginsenoside Rg1 had a significant protective effect on focal cerebral I/R injury in middle cerebral artery occlusion (MCAO) rats. However, the mechanism still needs further clarification. Here, we firstly reported that ginsenoside Rg1 effectively suppressed the inflammatory activation of brain microglia cells under I/R conditions depending on the inhibition of Toll-likereceptor4 (TLR4) proteins. In vivo experiments showed that the ginsenoside Rg1 administration could significantly improve the cognitive function of MCAO rats, and in vitro experimental data showed that ginsenoside Rg1 significantly alleviated neuronal damage via inhibiting the inflammatory response in microglia cells co-cultured under oxygen and glucose deprivation/reoxygenation (OGD/R) condition in gradient dependent. The mechanism study showed that the effect of ginsenoside Rg1 depends on the suppression of TLR4/MyD88/NF-κB and TLR4/TRIF/IRF-3 pathways in microglia cells. In a word, our research shows that ginsenoside Rg1 has great application potential in attenuating the cerebral I/R injury by targeting TLR4 protein in the microglia cells.
Insights
Ginsenoside Rg1 protects against cerebral ischemia/reperfusion injury by inhibiting microglia inflammation via the Toll-like receptor 4 pathway. This compound shows potential for treating brain injury by targeting microglia activation.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Cerebral ischemia/reperfusion (I/R) injury involves microglia-driven inflammation and neuronal damage.
- Ginsenoside Rg1 demonstrated protective effects in previous studies on focal cerebral I/R injury.
- The precise mechanism of ginsenoside Rg1's neuroprotection requires further elucidation.
Purpose of the Study:
- To investigate the mechanism by which ginsenoside Rg1 mitigates cerebral I/R injury.
- To determine if ginsenoside Rg1 suppresses inflammatory activation of microglia.
- To explore the role of Toll-like receptor 4 (TLR4) in ginsenoside Rg1's protective effects.
Main Methods:
- In vivo studies using middle cerebral artery occlusion (MCAO) rat models.
- In vitro experiments with microglia cells under oxygen and glucose deprivation/reoxygenation (OGD/R).
- Analysis of TLR4, MyD88, NF-κB, TRIF, and IRF-3 signaling pathways.
Main Results:
- Ginsenoside Rg1 significantly improved cognitive function in MCAO rats.
- Ginsenoside Rg1 alleviated neuronal damage in OGD/R-treated microglia co-cultures.
- Ginsenoside Rg1 inhibited microglia inflammatory activation by suppressing TLR4/MyD88/NF-κB and TLR4/TRIF/IRF-3 pathways.
Conclusions:
- Ginsenoside Rg1 effectively suppresses microglia inflammatory activation in cerebral I/R injury.
- The protective mechanism involves the inhibition of the TLR4 signaling pathway in microglia.
- Ginsenoside Rg1 exhibits significant potential for attenuating cerebral I/R injury by targeting TLR4.
