2014
DOI: 10.1007/s12028-014-0010-z
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Rosiglitazone Attenuates Cerebral Vasospasm and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage

Abstract: Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.

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Cited by 14 publications
(8 citation statements)
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“…A study indeed showed rosiglitazone‐mediated GFAP increase, but in terms of restored astrocyte activity in subarachnoid hemorrhage (Lin et al . ). On the other hand, our observations in the diabetic brain closely emulated the effects of rosiglitazone against striatal dopaminergic neurodegeneration (Lee et al .…”
Section: Discussionmentioning
confidence: 97%
See 1 more Smart Citation
“…A study indeed showed rosiglitazone‐mediated GFAP increase, but in terms of restored astrocyte activity in subarachnoid hemorrhage (Lin et al . ). On the other hand, our observations in the diabetic brain closely emulated the effects of rosiglitazone against striatal dopaminergic neurodegeneration (Lee et al .…”
Section: Discussionmentioning
confidence: 97%
“…Additionally, roziglitazone attenuated GFAP loss and enhanced astrocyte activity after cerebral hemorrhage (Lin et al . ). Nonetheless, rosiglitazone‐induced mechanism in astrocytes remains less investigated.…”
mentioning
confidence: 97%
“…Rosiglitazone is a highly selective and potent agonist to peroxisome proliferator-activated receptor γ . Continuous treatment with 6 mg/kg rosiglitazone for 6 days reduces glutamate level, upregulates GLT-1 expression, reduces MDA and catalase levels, and ameliorates vasospasm following SAH, exhibiting a protective role in the brain [ 161 ]. Treatment with rosiglitazone in cerebral hemorrhage regulates antioxidation and anti-inflammatory effects, possibly through the interaction of Nrf-2, retinoid X receptor (RXR), and NF- κ B and reduces SBI [ 162 ].…”
Section: Antioxidant Therapy After Ichmentioning
confidence: 99%
“…In the literature, different experimental models have shown that rosiglitazone has protective and antiapoptotic effects on both neural stem cells (NSCs) and mature neurons by preventing the glial-induced inflammation or regulating the intercellular pathways. In ischemia-reperfusion-induced and traumatic brain injury animal models, [22][23][24][25][26][27][28] rosiglitazone has been reported to suppress the glial inflammatory cytokine production (TNFa and IL-1) through the over-activation of glial cells (astrocyte or microglia). This finding correlates with the reduction in neuronal death rates in the hippocampus or other brain areas.…”
Section: Discussionmentioning
confidence: 99%