ArticleExperimental and therapeutic medicine2016
Rosiglitazone ameliorates astrocyte over-activation and inflammatory cytokine release induced by global cerebral ischemia/reperfusion.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 10 citations in OpenAlex.
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- Pseudane-VII Regulates LPS-Induced Neuroinflammation in Brain Microglia Cells through the Inhibition of iNOS Expression.Molecules (Basel, Switzerland) · 2018Article
- 3'-Daidzein sulfonate sodium provides neuroprotection by promoting the expression of the α7 nicotinic acetylcholine receptor and suppressing inflammatory responses in a rat model of focal cerebral ischemia.American journal of translational research · 2018Article
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4 authors at 2 institutions in 1 country.
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Abstract
Global cerebral ischemia (GCI) is a leading cause of mortality worldwide and remains the primary cause of long-term neurological disability. Astrocyte over-activation and extensive neuron loss in the ischemic brain are the characteristic pathological features of cerebral ischemia. Rosiglitazone (RSG) is a peroxisome-proliferating activating receptor-γ agonist known for its anti-inflammatory activity. Previous studies have suggested that RSG is able to exert neuroprotection in numerous acute and chronic brain injury models. However, whether RSG treatment is involved in astrocyte over-activation and inflammatory reaction in the cortex remains unclear. The aim of the present study was to investigate whether RSG treatment improved functional impairment induced following GCI and protected against cortex neuron loss, and to elucidate the potential mechanisms underlying these functions. Rats were randomly divided into three groups: Sham-operated, GCI and RSG treatment groups. The RSG treatment group was treated with 2 mg/kg RSG immediately following GCI. The results demonstrated that RSG treatment significantly reduced infarct volume and neuron survival rates in addition to increasing function recovery. Furthermore, these results correlate with a reduction in astrocyte over-activation and inflammatory cytokines in the rat cortex. However, no significant changes in glutamate transporter-1 expression levels were observed following RSG treatment compared with the GCI rats. The results of this investigation provide
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