4.4 Article

Effects of borneol combined with astragaloside IV and Panax notoginseng saponins regulation of microglia polarization to promote neurogenesis after cerebral ischaemia

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JOURNAL OF PHARMACY AND PHARMACOLOGY
卷 75, 期 7, 页码 940-950

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OXFORD UNIV PRESS
DOI: 10.1093/jpp/rgad033

关键词

cerebral ischaemia-reperfusion; neurogenesis; microglia polarization; inflammatory microenvironment; NF kappa B; borneol combined with AST IV and PNS

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The study aimed to investigate the effect of BAP on promoting neurogenesis by regulating microglia polarization after CI/R in rats. BAP can inhibit the activation of TLR4/MyD88/NF kappa B, regulate the polarization of microglia from M1 type to M2 type, and inhibit inflammatory response, thus reducing CI/R injury and promoting neurogenesis.
Objective To study the effect of borneol combined with astragaloside IV and Panax notoginseng saponins (BAP) on promoting neurogenesis by regulating microglia polarization after cerebral ischaemia-reperfusion(CI/R) in rats. Methods A focal CI/R injury model was established. Evaluated the effects of BAP on ischaemic brain injury, on promoting neurogenesis, on inhibiting Inflammatory microenvironment and TLR4/MyD88/NF kappa B signalling pathway. A microglia oxygen-glucose deprivation reoxygenation (OGD/R) model was established that evaluated the effects of BAP on regulating the polarization of microglia and inflammatory microenvironment. Results BAP can inhibit the expression of TLR4, MyD88 and NF kappa B proteins, reduce IL-1 beta and increase IL-10, reduce M1 type microglia and increase M2 microglia. The proliferation of neural stem cells increased, synaptic gap decreased, synaptic interface curvature increased, expression of SYN and PSD95 proteins increased, which improved the neurological dysfunction and reduced the volume of cerebellar infarction and nerve cell injury. Conclusion BAP can reduce CI/R injury and promote neurogenesis, the effect is related to inhibition of the activation of TLR4/MyD88/NF kappa B, regulating the polarization of microglia from M1 type to M2 type and inhibition of inflammatory response.

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