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Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced bv2 microglia

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Chinese Journal of Natural Medicines 2017年第9期15卷 674-679页

作者： WANG Li-Chao LIAO Li-Xi ZHAO Ming-Bo DONG Xin ZENG Ke-Wu TU Peng-Fei State Key Laboratory of Natural and Biomimetic Drugs School of Pharmaceutical Sciences Peking University State Key Laboratory of Natural Medicines China Pharmaceutical University

microglial activation and resultant neuroinflammatory response are implicated in various brain diseases including Alzheimer's disease and Parkinson's disease. Treatment with anti-neuroinflammatory agents could provide therapeutic benefits for such disorders. Protosappanin A(PTA) is a major bioactive ingredient isolated from Caesalpinia sappan L.. In this work, the anti-neuroinflammatory effects of PTA on LPS-stimulated bv2 cells were investigated and the underlying mechanisms were explored. Results showed that PTA significantly inhibited the production of TNF-α and IL-1β in LPS-activated bv2 microglia. Moreover, the mR NA expressions of IL-6, IL-1β, and MCP-1 were reduced by PTA in a dose-dependent manner. Furthermore, PTA suppressed JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3, as well as STAT3 nuclear translocation against LPS treatment. These observations suggested a novel role for PTA in regulating LPS-induced neuroinflammatory injuries.

关键词： Neuroinflammation bv2 microglia Lipopolysaccharide Protosappanin A JAK2-STAT3

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Exosomes derived from bone marrow mesenchymal stem cells inhibit neuroinflammation after traumatic brain injury

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Neural Regeneration Research 2022年第12期17卷 2717-2724页

作者： Liang Wen Ya-Dong Wang Dong-Feng Shen Pei-Dong Zheng Meng-Di Tu Wen-Dong You Yuan-Run Zhu Hao Wang Jun-Feng Feng Xiao-Feng Yang The First Affiliated Hospital School of MedicineZhejiang UniversityHangzhouZhejiang ProvinceChina Department of Intensive Care Unit The First Hospital of JiaxingJiaxingZhejiang ProvinceChina Department of Neurosurgery Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina

Exosomes derived from bone marrow mesenchymal stem cells can inhibit neuroinflammation through regulating microglial phenotypes and promoting nerve injury repair.However,the underlying molecular mechanism remains unclear.In this study,we investigated the mechanism by which exosomes derived from bone marrow mesenchymal stem cells inhibit neuroinflammation.Our in vitro co-culture experiments showed that bone marrow mesenchymal stem cells and their exosomes promoted the polarization of activated bv2 microglia to their anti-inflammatory phenotype,inhibited the expression of proinflammatory cytokines,and increased the expression of anti-inflammatory cytokines.Our in vivo experiments showed that tail vein injection of exosomes reduced cell apoptosis in cortical tissue of mouse models of traumatic brain injury,inhibited neuroinflammation,and promoted the transformation of microglia to the anti-inflammatory phenotype.We screened some microRNAs related to neuroinflammation using microRNA sequencing and found that microRNA-181b seemed to be actively involved in the process.Finally,we regulated the expression of miR181b in the brain tissue of mouse models of traumatic brain injury using lentiviral transfection.We found that miR181b overexpression effectively reduced apoptosis and neuroinflamatory response after traumatic brain injury and promoted the transformation of microglia to the anti-inflammatory phenotype.The interleukin 10/STAT3 pathway was activated during this process.These findings suggest that the inhibitory effects of exosomes derived from bone marrow mesenchymal stem cells on neuroinflamation after traumatic brain injury may be realized by the action of miR181b on the interleukin 10/STAT3 pathway.

关键词： apoptosis bone marrow mesenchymal stem cells bv2 microglia exosome interleukin 10 lentiviral transfection microRNA-181b neuroinflammation phenotype signal transducer and activator of transcription 3 traumatic brain injury

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