• Publications
  • Influence
Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage.
TLDR
It was observed that an ATX intracerebroventricular injection 30 minutes post-SAH could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological dysfunction) after SAH in rats, and ATX treatment could prevent oxidative damage and upregulate the endogenous antioxidant levels in the rat cerebral cortex following SAH. Expand
Peroxiredoxin 2 activates microglia by interacting with Toll-like receptor 4 after subarachnoid hemorrhage
TLDR
Extracellular Prx2 in CSF after SAH is a DAMP which resulted in microglial activation via TLR4/MyD88/NF-κB pathway and then neuronal apoptosis and may be a potential indicator of brain injury and prognosis. Expand
Peroxiredoxin 1/2 protects brain against H2O2‐induced apoptosis after subarachnoid hemorrhage
  • Y. Lu, X. Zhang, +8 authors C. Hang
  • Biology, Medicine
  • FASEB journal : official publication of the…
  • 1 February 2019
TLDR
Early expression of Prx1/2 may protect the brain from oxidative damage after SAH and may provide a novel target for treating SAH, and protects brain against H2O2‐induced apoptosis after subarachnoid hemorrhage. Expand
Puerarin ameliorates oxidative stress in a rodent model of traumatic brain injury.
TLDR
Results indicate that puerarin can ameliorate oxidative neurodegeneration after TBI, at least in part, through the activation of PI3K-Akt pathway. Expand
Astaxanthin Alleviates Early Brain Injury Following Subarachnoid Hemorrhage in Rats: Possible Involvement of Akt/Bad Signaling
TLDR
The results provided the evidence that ATX could attenuate apoptosis in a rat SAH model, potentially, in part, through modulating the Akt/Bad pathway. Expand
Activation of Nuclear Factor-κB in the Brain after Experimental Subarachnoid Hemorrhage and Its Potential Role in Delayed Brain Injury
TLDR
It is demonstrated that the activated NF-κB in neurons after SAH plays an important role in regulating the expressions of inflammatory genes in the brain, and ultimately contributes to delayed brain injury. Expand
Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll‐like receptor 4 signaling pathway
  • X. Zhang, Y. Lu, +7 authors J. Wang
  • Medicine
  • FASEB journal : official publication of the…
  • 1 January 2019
TLDR
Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll‐like receptor 4 signaling pathway, and reduces the proinflammatory response and secondary brain injury after SAH. Expand
Activation of metabotropic glutamate receptor 5 reduces the secondary brain injury after traumatic brain injury in rats.
TLDR
The data indicated that post-TBI treatment with CHPG could significantly reduce the secondary brain injury characterized by the cerebral edema and neuronal degeneration, lead to the inhibition of microglia activation and decrease the expression of pro-inflammatory cytokines in both mRNA transcription and protein synthesis. Expand
Inhibition of c-Jun N-terminal Kinase Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Through Inhibition of a Nur77 Dependent Apoptosis Pathway
TLDR
The hypothesis that SP600125 treatment can ameliorate EBI after experimentally induced SAH by inhibiting a Nur77-dependent apoptotic pathway is supported. Expand
N-acetylcysteine amide provides neuroprotection via Nrf2-ARE pathway in a mouse model of traumatic brain injury
TLDR
NACA potentially provides neuroprotection via the activation of the Nrf2-ARE signaling pathway after TBI in mice, and treatment with NACA significantly improved neurologic status at days 1 and 3 following TBI. Expand
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