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Expression of the NLRP3 Inflammasome in Cerebral Cortex After Traumatic Brain Injury in a Rat Model
TLDR
The results showed that, TBI could induce assembly of NLRP3-inflammasome complex, increased expression of ASC, activation of caspase1, and processing of IL-1β and IL-18, which suggested that NLRP 3-infammasome might play an important role in the inflammation induced by TBI and could be a target for TBI therapy. Expand
Cerebrovascular Dysfunction in Amyloid Precursor Protein Transgenic Mice: Contribution of Soluble and Insoluble Amyloid-β Peptide, Partial Restoration via γ-Secretase Inhibition
TLDR
The results strongly suggest that both soluble and insoluble Aβ cause cerebrovascular dysfunction, that mechanisms other than Aβ-induced alteration in vessel integrity are responsible, and that anti-Aβ therapy may have beneficial vascular effects in addition to positive effects on parenchymal amyloid. Expand
Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice
TLDR
Evidence is demonstrated that reactive oxygen species (ROS) and, in particular, NADPH oxidase-derived ROS are a key mediator of CAA-induced CV deficits and a promising therapeutic target for patients with CAA and AD. Expand
Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro
TLDR
Results demonstrated HMGB1 translocation occurred as early as 2 h after experimental SAH with mRNA and protein level increased and might trigger inflammation as an upstream inflammatory mediator. Expand
Melatonin stimulates antioxidant enzymes and reduces oxidative stress in experimental traumatic brain injury: the Nrf2-ARE signaling pathway as a potential mechanism.
TLDR
Melatonin administration may increase the activity of antioxidant enzymes and attenuate brain injury in a TBI model, potentially via mediation of the Nrf2-ARE pathway. Expand
Potential Contribution of Nuclear Factor-κB to Cerebral Vasospasm after Experimental Subarachnoid Hemorrhage in Rabbits
TLDR
The results suggest that NF-κB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response. Expand
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
Sirtuin 1 activation protects against early brain injury after experimental subarachnoid hemorrhage in rats
TLDR
The results suggest that SIRT1 plays an important role in neuroprotection against EBI after SAH by deacetylation and subsequent inhibition of forkhead transcription factors of the O class, nuclear factor-kappa B- and p53-induced oxidative, inflammatory and apoptotic pathways. Expand
Phosphodiesterase 5 Inhibition Attenuates Cerebral Vasospasm and Improves Functional Recovery After Experimental Subarachnoid Hemorrhage
TLDR
Sildenafil, a US Food and Drug Administration–approved drug with a proven track record of safety in humans, is a promising new therapy for vasospasm and neurological deficits after SAH. Expand
Hydrogen-rich saline alleviates early brain injury via reducing oxidative stress and brain edema following experimental subarachnoid hemorrhage in rabbits
TLDR
The results suggest that treatment with hydrogen in experimental SAH rabbits could alleviate brain injury via decreasing the oxidative stress injury and brain edema, and conclude that hydrogen possesses the potential to be a novel therapeutic agent for EBI after SAH. Expand
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