http://purl.uniprot.org/citations/32645874 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/32645874 | http://www.w3.org/2000/01/rdf-schema#comment | "Acute ischemic stroke (AIS) is a devastating neurological condition with a lack of neuroprotective therapeutic options, despite the reperfusion modalities thrombolysis and thrombectomy. Post-ischemic brain damage is aggravated by an excessive inflammatory cascade involving the activation and regulation of the pro-inflammatory cytokines IL-1β and IL-18 by inflammasomes. However, the role of AIM2 and NLRC4 inflammasomes and the influence of the neuroprotective steroids 17β-estradiol (E2) and progesterone (P) on their regulation after ischemic stroke have not yet been conclusively elucidated. To address the latter, we subjected a total of 65 rats to 1 h of transient Middle Cerebral Artery occlusion (tMCAO) followed by a reperfusion period of 72 h. Moreover, we evaluated the expression and regulation of AIM2 and NLRC4 in glial single-cell cultures (astroglia and microglia) after oxygen-glucose deprivation (OGD). The administration of E2 and P decreased both infarct sizes and neurological impairments after cerebral ischemia in rats. We detected a time-dependent elevation of gene and protein levels (Western Blot/immunohistochemistry) of the AIM2 and NLRC4 inflammasomes in the post-ischemic brains. E2 or P selectively mitigated the stroke-induced increase of AIM2 and NLRC4. While both inflammasomes seemed to be exclusively abundant in neurons under physiological and ischemic conditions in vivo, single-cell cultures of cortical astrocytes and microglia equally expressed both inflammasomes. In line with the in vivo data, E and P selectively reduced AIM2 and NLRC4 in primary cortical astrocytes and microglial cells after OGD. In conclusion, the post-ischemic elevation of AIM2 and NLRC4 and their down-regulation by E2 and P may shed more light on the anti-inflammatory effects of both gonadal hormones after stroke."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.org/dc/terms/identifier | "doi:10.3390/ijms21134795"xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/author | "Slowik A."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/author | "Harms J."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/author | "Beyer C."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/author | "Habib P."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/author | "Zendedel A."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/name | "Int J Mol Sci"xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/pages | "E4795"xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/title | "Gonadal Hormones E2 and P Mitigate Cerebral Ischemia-Induced Upregulation of the AIM2 and NLRC4 Inflammasomes in Rats."xsd:string |
http://purl.uniprot.org/citations/32645874 | http://purl.uniprot.org/core/volume | "21"xsd:string |
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