{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T17:45:19Z","timestamp":1788371119742,"version":"build-2803163510"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,8,7]],"date-time":"2025-08-07T00:00:00Z","timestamp":1754524800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Synapse"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Isoflurane (ISO) exposure is associated with neuroinflammation and postoperative cognitive dysfunction (POCD) in aged populations, although the underlying mechanisms remain unclear. This study aimed to determine whether ISO\u2010induced cognitive decline involves miR\u2010365a\u20103p and its downstream signaling targets. Aged rats were exposed to ISO to establish a POCD model. Cognitive and motor functions were evaluated using Morris water maze tests and neurological scoring. The expression of miR\u2010365a\u20103p, inflammatory factors, synaptic proteins, and apoptotic markers in the hippocampus was measured by qRT\u2010PCR, ELISA, and Western blotting. In vitro, LPS\u2010treated BV\u20102 microglia were co\u2010cultured with differentiated SH\u2010SY5Y neurons to assess neuronal apoptosis rate (by flow cytometry) and synaptic integrity. Dual\u2010luciferase reporter assays verified the direct interaction between miR\u2010365a\u20103p and MyD88. ISO exposure reduced hippocampal miR\u2010365a\u20103p, resulting in memory\/motor deficits, increased pro\u2010inflammatory factors, microglial activation, synaptic protein loss, and neuronal apoptosis. Adding extra miR\u2010365a\u20103p reversed these problems. LPS treatment reduced miR\u2010365a\u20103p expression and enhanced pro\u2010inflammatory cytokine production in BV\u20102 cells, which subsequently induced apoptosis in co\u2010cultured neurons and impaired synaptic integrity. These conditions were reversed by miR\u2010365a\u20103p overexpression. Mechanistically, miR\u2010365a\u20103p directly targeted MyD88, inhibiting its expression and downstream NF\u2010\u03baB activation. MyD88 overexpression reversed protective effects of miR\u2010365a\u20103p on inflammation and synaptic function. ISO causes POCD by reducing miR\u2010365a\u20103p, which protects the brain by blocking MyD88\/NF\u2010\u03baB. Boosting miR\u2010365a\u20103p may represent a potential strategy to help prevent ISO\u2010related brain harm in elderly patients, warranting further translational investigation.<\/jats:p>","DOI":"10.1002\/syn.70025","type":"journal-article","created":{"date-parts":[[2025,8,7]],"date-time":"2025-08-07T10:00:08Z","timestamp":1754560808000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["miR\u2010365a\u20103p Alleviates Isoflurane\u2010Induced Neuroinflammation and Cognitive Impairment by Targeting MyD88 to Inhibit NF\u2010\u03baB Signaling"],"prefix":"10.1002","volume":"79","author":[{"given":"Shujuan","family":"Bai","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Xianyang Hospital Yan'an University  Xianyang 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