{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:02:26Z","timestamp":1789970546091,"version":"4.0.1"},"reference-count":53,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:00:00Z","timestamp":1789948800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Icariside II (ICS II), a major bioactive flavonoid metabolite from\n                      <jats:italic>Epimedium<\/jats:italic>\n                      , has been reported to exert neuroprotective effects, but its role in regulating mitochondrial dysfunction-related neuronal injury in Alzheimer\u2019s disease (AD) has not been fully clarified.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this study, we administered ICS II to APP\/PS1 transgenic mice and to two neuronal cell models of AD-like injury (A\u03b2-exposed HT22 cells and APP-overexpressing N2a cells). We evaluated cognitive behaviour, histopathological changes, A\u03b2 burden, neuronal apoptosis, mitochondrial membrane potential (\u0394\u03a8m), mitochondrial reactive oxygen species (mtROS) levels, mitochondrial morphology and dynamics (including fragmentation, mitofusin-2 (Mfn2) expression, and dynamin-related protein 1 (Drp1) phosphorylation), as well as cytochrome c (Cyt c) release and caspase-3 activity. RNA-sequencing analysis of hippocampal tissue and pharmacological inhibition with the PI3K inhibitor LY294002 were employed to probe the involvement of the PI3K\/AKT signalling pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and discussion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>In vivo<\/jats:italic>\n                      , ICS II improved cognitive performance, ameliorated hippocampal and cortical histopathological damage, decreased A\u03b2 immunoreactivity, and reduced neuronal apoptosis. RNA-sequencing analysis suggested the involvement of PI3K\/AKT signaling in the response to ICS II treatment.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , ICS II increased cell viability, reduced oxidative stress, and inhibited apoptosis. These effects were associated with increased PI3K expression and AKT phosphorylation, restoration of \u0394\u03a8m, reduced mtROS accumulation, restored mitochondrial morphology (e.g., alleviated fragmentation, reduced punctate fragments, and increased mitochondrial length), decreased Cyt c release, increased Mfn2 expression, and decreased Drp1 phosphorylation at Ser616 and caspase-3 levels. Notably, co-treatment with LY294002 largely abolished these protective effects, indicating that PI3K\/AKT signaling is functionally involved in this process. Taken together, our findings suggest that ICS II protects against AD-related neuronal injury are closely associated with PI3K\/AKT-dependent regulation of mitochondrial dynamics and apoptosis, thereby providing a mechanistic foundation for further exploration of ICS II as a natural product-derived candidate for AD intervention.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1911518","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T05:36:47Z","timestamp":1789969007000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Icariside II protects against neuronal injury by modulating PI3K\/AKT-dependent mitochondrial dynamics and apoptosis in Alzheimer\u2019s disease models"],"prefix":"10.3389","volume":"17","author":[{"given":"Si-Yu","family":"Shan","sequence":"first","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia-Ming","family":"Bai","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Tian","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Feng","family":"Shen","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ye-Xin","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Han","family":"Cheng","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Liu","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong-Yang","family":"Ning","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-Yu","family":"Min","sequence":"additional","affiliation":[{"name":"Traditional Chinese Medicine Experimental Center, Affiliated Hospital of Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Ren","sequence":"additional","affiliation":[{"name":"Mental Disorders Research Laboratory, Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong-He","family":"Xiao","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Liaoning University of Traditional Chinese Medicine","place":["Dalian, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,21]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1546256","DOI":"10.3389\/fphar.2025.1546256","article-title":"The active metabolite of epimedii folium promotes hippocampal neurogenesis in APP\/PS1 mice by alleviating mitochondrial dysfunction","volume":"16","author":"Bai","year":"2025","journal-title":"Front. 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