<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Stanojlovic M</submitter><funding>Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja</funding><pagination>829-843</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11448933</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(5)</volume><pubmed_abstract>Sustained activation of pro-apoptotic signaling due to a sudden and prolonged disturbance of cerebral blood circulation governs the neurodegenerative processes in prefrontal cortex (PFC) of rats whose common carotid arteries are permanently occluded. The adequate neuroprotective therapy should minimize the activation of toxicity pathways and increase the activity of endogenous protective mechanisms. Several neuroprotectants have been proposed, including progesterone (P&lt;sub>4&lt;/sub>). However, the underlying mechanism of its action in PFC following permanent bilateral occlusion of common carotid arteries is not completely investigated. We, thus herein, tested the impact of post-ischemic P&lt;sub>4&lt;/sub> treatment (1.7 mg/kg for seven consecutive days) on previously reported aberrant neuronal mo</pubmed_abstract><journal>Cellular and molecular neurobiology</journal><pubmed_title>Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS.</pubmed_title><pmcid>PMC11448933</pmcid><funding_grant_id>41014</funding_grant_id><funding_grant_id>173044</funding_grant_id><pubmed_authors>Stanojlovic M</pubmed_authors><pubmed_authors>Mitrovic N</pubmed_authors><pubmed_authors>Martinovic J</pubmed_authors><pubmed_authors>Zaric M</pubmed_authors><pubmed_authors>Gusevac Stojanovic I</pubmed_authors><pubmed_authors>Grkovic I</pubmed_authors><pubmed_authors>Drakulic D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS.</name><description>Sustained activation of pro-apoptotic signaling due to a sudden and prolonged disturbance of cerebral blood circulation governs the neurodegenerative processes in prefrontal cortex (PFC) of rats whose common carotid arteries are permanently occluded. The adequate neuroprotective therapy should minimize the activation of toxicity pathways and increase the activity of endogenous protective mechanisms. Several neuroprotectants have been proposed, including progesterone (P&lt;sub>4&lt;/sub>). However, the underlying mechanism of its action in PFC following permanent bilateral occlusion of common carotid arteries is not completely investigated. We, thus herein, tested the impact of post-ischemic P&lt;sub>4&lt;/sub> treatment (1.7 mg/kg for seven consecutive days) on previously reported aberrant neuronal mo</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2025-04-22T18:57:41.833Z</modification><creation>2025-04-06T02:37:20.533Z</creation></dates><accession>S-EPMC11448933</accession><cross_references><pubmed>31865501</pubmed><doi>10.1007/s10571-019-00777-2</doi></cross_references></HashMap>