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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
Ginkgolide B Protects Against Ischemic Stroke Via Modulating Microglia Polarization in Mice
Zhao-Ma Shu1, Xiao-Dong Shu1, Hui-Qin Li2
1Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu, 210029, China.
Aim:
Ginkgolide B (GB) has shown neuroprotective effect in treating ischemic stroke, related to its property of anti-inflammation. Nevertheless, it is unclear whether GB is able to modulate microglia/macrophage polarization, which has recently been proven to be vital in the pathology of ischemic stroke.
Methods:
We performed transient middle cerebral artery occlusion (tMCAO) on C57BL/6J male mice and induced cultured BV2 microglia and primary bone marrow-derived macrophages to be M1/2 phenotype by LPS+ interferon-γ and IL-4, respectively. Immunofluorescence and flow cytometry were used for detecting the specialized protein expression of M1/2, such as CD206 and CD16/32. qPCR was utilized to detect the signature gene change of M1/2.
Results:
GB significantly reduced cerebral ischemic damage and ameliorated the neurological deficits of mice after tMCAO. More importantly, our experiments proved that GB promoted microglia/macrophage transferring from inflammatory M1 phenotype to a protective, anti-inflammatory M2 phenotype in vivo or vitro. CV3988 and silencing the platelet activator factor (PAF) receptor by siRNA demonstrated that PAF receptor was involved in the modulation of microglia/macrophage polarization.
Conclusion:
Our results reveal a novel pharmacological effect of GB in modulating microglia/macrophage polarization after tMCAO, thus deepening our understanding of neuroprotective mechanisms of GB in treatment of ischemic stroke. Furthermore, this new mechanism may allow GB to be used in many other microglia/macrophage polarization-related inflammatory diseases.
Insights
Ginkgolide B (GB) mitigates ischemic stroke damage by shifting microglia/macrophages from inflammatory M1 to protective M2 states, revealing a novel neuroprotective mechanism.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Ginkgolide B (GB) exhibits neuroprotective effects in ischemic stroke, linked to anti-inflammatory properties.
- The role of GB in modulating microglia/macrophage polarization, crucial in ischemic stroke pathology, remains unclear.
Purpose of the Study:
- To investigate Ginkgolide B's effect on microglia/macrophage polarization in the context of ischemic stroke.
- To elucidate the underlying mechanisms of GB's neuroprotective action.
Main Methods:
- Transient middle cerebral artery occlusion (tMCAO) model in mice.
- In vitro induction of M1/M2 phenotypes in BV2 microglia and bone marrow-derived macrophages.
- Immunofluorescence, flow cytometry, and qPCR for analyzing M1/M2 markers and gene expression.
Main Results:
- GB significantly reduced cerebral ischemic damage and neurological deficits post-tMCAO.
- GB promoted the shift of microglia/macrophages from M1 to M2 phenotype both in vivo and in vitro.
- Platelet-activating factor (PAF) receptor was identified as involved in GB-mediated polarization modulation.
Conclusions:
- GB demonstrates a novel pharmacological effect in modulating microglia/macrophage polarization after ischemic stroke.
- This finding deepens the understanding of GB's neuroprotective mechanisms in ischemic stroke treatment.
- The identified mechanism suggests potential therapeutic applications of GB in other inflammatory diseases involving microglia/macrophage polarization.
