Astragaloside Improves Outcomes of Traumatic Brain Injury in Rats by Reducing Microglia Activation

Astragaloside (AST) is traditionally prescribed for the prevention and treatment of cerebrovascular diseases. We directly tested the therapeutic effects of AST in a rat model of traumatic brain injury (TBI). One hour after the onset of TBI rats were given Saline (1 ml/kg) or AST (20–80 mg/kg) via i.p. injection. AST causes the attenuation of TBI-induced cerebral contusion, neuronal apoptosis, and neurological motor dysfunction. TBI-induced microglial activation evidenced by the morphological transformation of microglia (or ameboid microglia) and the microglial overexpression of tumor necrosis factor-alpha was reduced by AST. Our results indicate that AST may protect against brain contusion and neuronal apoptosis after TBI by attenuating microglia activation in male rats.

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Enriching neural stem cell and anti‐inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats

Journal of Neuroscience Research ◽

10.1002/jnr.24834 ◽

2021 ◽

Author(s):

Eunyoung Park ◽

Johnathan G. Lyon ◽

Melissa Alvarado‐Velez ◽

Martha I. Betancur ◽

Nassir Mokarram ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Stem Cell ◽

Electrical Stimulation ◽

Brain Injury ◽

Neural Stem Cell ◽

Male Rats ◽

Anti Inflammatory

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FGF10 Attenuates Experimental Traumatic Brain Injury through TLR4/MyD88/NF-κB Pathway

Cells Tissues Organs ◽

10.1159/000511381 ◽

2021 ◽

pp. 1-9

Author(s):

Qinhan Hou ◽

Hongmou Chen ◽

Quan Liu ◽

Xianlei Yan

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Protein Expression ◽

Water Content ◽

Neurological Deficit ◽

Neuronal Apoptosis ◽

Neuronal Damage ◽

Intraventricular Injection ◽

Brain Water Content ◽

Brain Water

Traumatic brain injury (TBI) can induce neuronal apoptosis and neuroinflammation, resulting in substantial neuronal damage and behavioral disorders. Fibroblast growth factors (FGFs) have been shown to be critical mediators in tissue repair. However, the role of FGF10 in experimental TBI remains unknown. In this study, mice with TBI were established via weight-loss model and validated by increase of modified neurological severity scores (mNSS) and brain water content. Secondly, FGF10 levels were elevated in mice after TBI, whereas intraventricular injection of Ad-FGF10 decreased mNSS score and brain water content, indicating the remittance of neurological deficit and cerebral edema in TBI mice. In addition, neuronal damage could also be ameliorated by stereotactic injection of Ad-FGF10. Overexpression of FGF10 increased protein expression of Bcl-2, while it decreased Bax and cleaved caspase-3/PARP, and improved neuronal apoptosis in TBI mice. In addition, Ad-FGF10 relieved neuroinflammation induced by TBI and significantly reduced the level of interleukin 1β/6, tumor necrosis factor α, and monocyte chemoattractant protein-1. Moreover, Ad-FGF10 injection decreased the protein expression level of Toll-like receptor 4 (TLR4), MyD88, and phosphorylation of NF-κB (p-NF-κB), suggesting the inactivation of the TLR4/MyD88/NF-κB pathway. In conclusion, overexpression of FGF10 could ameliorate neurological deficit, neuronal apoptosis, and neuroinflammation through inhibition of the TLR4/MyD88/NF-κB pathway, providing a potential therapeutic strategy for brain injury in the future.

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