Berberine Facilitates Angiogenesis Against Ischemic Stroke Through Modulating Microglial Polarization via AMPK Signaling

Zhu, Junrong; Cao, Ding-wen; Guo, Chao; Liu, Manman; Tao, Yifu; Zhou, Junshan; Wang, Rui; Zhao, Yanli; Wei, Jing; Zhang, Yingdong; Fang, Weirong; Li, Yunman

doi:10.1007/s10571-019-00675-7

Cited by 81 publications

(71 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on these changes, it is possible to draw some useful conclusions regarding ischemic stroke. For example, in MCAO mice, the expression levels of certain proinflammatory cytokines, such as il-1β, TnF-α and il-6, in addition to inoS, were observed to increase from 12 h, peak at day 14, then subsequently decrease and remain constant in the ischemic boundary zone until day 28 following Mcao (25,43). in addition, the study (25) also observed that CD32 expression levels increased in a similar manner.…”

Section: Microgliamentioning

confidence: 68%

“…For example, in MCAO mice, the expression levels of certain proinflammatory cytokines, such as il-1β, TnF-α and il-6, in addition to inoS, were observed to increase from 12 h, peak at day 14, then subsequently decrease and remain constant in the ischemic boundary zone until day 28 following Mcao (25,43). in addition, the study (25) also observed that CD32 expression levels increased in a similar manner. another previous study drew similar conclusions, witnessing a significant increase in CD16 expression levels from day 3, which remained elevated until day 14 in the cortex and striatum at the inner boundary of the infarct (44).…”

Section: Microgliamentioning

confidence: 68%

“…changes in the activation of M1 microglia can affect stroke prognosis and changes in the expression levels of M1 microglia biomarkers, including surface markers and proinflammatory cytokines, are also common in ischemic stroke (13,25,43). Based on these changes, it is possible to draw some useful conclusions regarding ischemic stroke.…”

Section: Microgliamentioning

confidence: 99%

See 2 more Smart Citations

Modulators of microglia activation and polarization in ischemic stroke (Review)

et al. 2020

View full text Add to dashboard Cite

ischemic stroke is one of the leading causes of mortality and disability worldwide. However, there is a current lack of effective therapies available. as the resident macrophages of the brain, microglia can monitor the microenvironment and initiate immune responses. in response to various brain injuries, such as ischemic stroke, microglia are activated and polarized into the proinflammatory M1 phenotype or the anti-inflammatory M2 phenotype. The immunomodulatory molecules, such as cytokines and chemokines, generated by these microglia are closely associated with secondary brain damage or repair, respectively, following ischemic stroke. it has been shown that M1 microglia promote secondary brain damage, whilst M2 microglia facilitate recovery following stroke. in addition, autophagy is also reportedly involved in the pathology of ischemic stroke through regulating the activation and function of microglia. Therefore, this review aimed to provide a comprehensive overview of microglia activation, their functions and changes, and the modulators of these processes, including transcription factors, membrane receptors, ion channel proteins and genes, in ischemic stroke. The effects of autophagy on microglia polarization in ischemic stroke were also reviewed. Finally, future research areas of ischemic stroke and the implications of the current knowledge for the development of novel therapeutics for ischemic stroke were identified. Contents 1. introduction 2. Microglia 3. Modulatory mechanisms of microglia polarization 4. autophagy 5. conclusions

show abstract

Section: Microgliamentioning

confidence: 68%

Section: Microgliamentioning

confidence: 68%

See 1 more Smart Citation

Modulators of microglia activation and polarization in ischemic stroke (Review)

et al. 2020

View full text Add to dashboard Cite

show abstract

“…When inflammation, infection, trauma or other neurological diseases occur in the brain, microglia become quickly activated and phagocytic. Under the influence of pathological damage factors of TBI, microglia convert from resting state into active state and secrete a large number of cytokines . Activated microglia are able to produce both pro‐inflammatory cytokines and anti‐inflammatory cytokines, and intervention of the inflammatory regulation of microglia is of vital significance for the treatment of CNS diseases …”

Section: Introductionmentioning

confidence: 99%

“…Under the influence of pathological damage factors of TBI, microglia convert from resting state into active state and secrete a large number of cytokines. [6] Activated microglia are able to produce both pro-inflammatory cytokines and anti-inflammatory cytokines, and intervention of the inflammatory regulation of microglia is of vital significance for the treatment of CNS diseases. [7][8][9] Brain-derived neurotrophic factor (BDNF) is one of the most important growth factors in CNS, [10] which plays a vital role in the development of CNS and neuronal plasticity.…”

Section: Introductionmentioning

confidence: 99%

Brain-derived neurotrophic factor fused with a collagen-binding domain inhibits neuroinflammation and promotes neurological recovery of traumatic brain injury mice via TrkB signalling

Yin

Zhao

Qiu

2020

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

Objectives As one of the vital nutrient factors in central nervous system (CNS), brain‐derived neurotrophic factor (BDNF) can significantly attenuate neuron damage and promote neurogenesis. Nevertheless, little research has been conducted on regulating the effect of BDNF on the inflammatory response after traumatic brain injury (TBI). Methods In this study, we used BDNF fused with a collagen‐binding domain (CBD‐BDNF) to maintain a sufficient concentration of BDNF in the TBI hemisphere, and then, the regulatory effects of BDNF and CBD‐BDNF on the inflammatory response of microglia were investigated both on a TBI mice model in vivo and LPS‐stimulated microglia experiment in vitro. Key findings The results revealed that BDNF and CBD‐BDNF had similar effects on attenuating the pro‐inflammatory reactions but promoting anti‐inflammatory responses of microglia induced by LPS in vitro. Furthermore, CBD‐BDNF significantly improved the neurological behaviours of TBI mice and alleviated the inflammatory reaction after TBI, while BDNF had weaker effects compared with those of CBD‐BDNF. Additionally, the TrkB inhibitor K252a significantly inhibited the above effects of CBD‐BDNF. Conclusions In conclusion, CBD‐BDNF can promote the anti‐inflammatory function of microglia and neurological recovery of TBI mice through TrkB signalling.

show abstract

Neuroprotective Treatments for Ischemic Stroke: Opportunities for Nanotechnology

Kong

Chu

Wang

2022

Adv Funct Materials

View full text Add to dashboard Cite

Stroke is one type of central nervous system (CNS) disease. It has high mortality and disability rates. [1] Generally, there are two types of strokes: ischemic stroke and hemorrhagic stroke. Ischemic stroke is caused by insufficient oxygen and blood supplies to the brain, while hemorrhagic stroke is caused by bleeding or leaky blood vessels. [2] More than 80% of stroke patients suffer from ischemic stroke. [3] Ischemic stroke mainly occurs in middle cerebral arteries followed by atherosclerosis that blocks blood transport to the brain, resulting in sudden interruption of local cerebral circulation. [4] This blockage causes ischemia, hypoxia, and malnutrition in the brain, resulting in a series of serious consequences, such as the overproduction of

show abstract

Berberine Facilitates Angiogenesis Against Ischemic Stroke Through Modulating Microglial Polarization via AMPK Signaling

Cited by 81 publications

References 47 publications

Modulators of microglia activation and polarization in ischemic stroke (Review)

Modulators of microglia activation and polarization in ischemic stroke (Review)

Brain-derived neurotrophic factor fused with a collagen-binding domain inhibits neuroinflammation and promotes neurological recovery of traumatic brain injury mice via TrkB signalling

Neuroprotective Treatments for Ischemic Stroke: Opportunities for Nanotechnology

Contact Info

Product

Resources

About