2026-10-12T22:03:33Z https://api.figshare.com/v2/oai

oai:figshare.com:article/34038216 2026-10-01T04:32:06Z category_696 portal_316 item_type_3 month_year_10_2026

Data Sheet 1_Astragaloside IV attenuates post-ischemic neuroinflammation associated with Treg-related regulation of CD86/CD206-associated brain myeloid phenotypic responses and PI3K/AKT signaling alterations.zip Hengtong An (22659860) Shuhan Guo (8655441) Shaoze Yang (25151883) Tianci Zhang (3223902) Xiaowen Li (317720) Zejun Ma (20388123) Yitong Wang (1463038) Ruotong Wang (12744665) Xiaohong Zhou (62510) Weijuan Gao (22659866) Genetic Immunology astragaloside IV brain myeloid cells ischemic stroke neuroinflammation PI3K/AKT signaling regulatory T cells Background<p>Ischemic stroke triggers persistent neuroinflammation, microglial activation, and peripheral immune changes that aggravate secondary brain injury. Astragaloside IV (AS-IV), a major bioactive constituent of Astragalus membranaceus, has neuroprotective and immunomodulatory effects, but its influence on Tregs and CD86/CD206-associated microglial phenotypic responses remains unclear.</p>Aim<p>This study investigated whether AS-IV attenuates post-ischemic neuroinflammation in association with Treg-related immune responses, PI3K/AKT signaling alterations, and CD86/CD206-associated brain myeloid phenotypic responses.</p>Materials and methods<p>A mouse middle cerebral artery occlusion (MCAO) model was established using the intraluminal filament method. Neurological deficits, infarct volume, and histopathological injury were evaluated after AS-IV treatment. Western blotting and ELISA were used to assess inflammatory cytokines and PI3K/AKT-associated signaling in ischemic brain tissue. Transcriptomic analysis identified AS-IV-related biological processes and pathways. Flow cytometry quantified CD4⁺CD25⁺FOXP3⁺ regulatory populations and additionally analyzed CD4⁺FOXP3⁺ populations in the spleen and cervical lymph nodes, together with CD86⁺/CD206⁺ phenotypic responses within the CD11b⁺CD45^low/int population in brain tissue. Immunofluorescence evaluated brain CD3⁺FOXP3⁺ signals and Iba1/CD86 or Iba1/CD206 double-positive signals. Anti-CD25 intervention was used to evaluate the involvement of Treg-related immune responses in AS-IV-associated effects.</p>Results<p>AS-IV reduced infarct volume, showed a trend toward improvement in neurological deficit scores, and alleviated histopathological injury after MCAO. It decreased IL-6 and TNF-α and increased IL-10 and TGF-β in ischemic brain tissue. Transcriptomic analysis identified changes associated with the PI3K/AKT signaling pathway and immune regulatory processes, while western blotting showed increased p-PI3K/PI3K and p-AKT/AKT ratios after AS-IV treatment. AS-IV increased Treg proportions in the spleen and cervical lymph nodes and increased CD3⁺FOXP3⁺ signals in brain tissue. It also reduced CD86⁺-associated and increased CD206⁺-associated brain myeloid phenotypic responses. Anti-CD25 partially attenuated AS-IV-associated improvements in neurological and brain injury outcomes, as well as its effects on inflammatory cytokines and brain myeloid phenotypic responses.</p>Conclusion<p>AS-IV attenuated post-ischemic neuroinflammation in association with Treg-related immune responses and PI3K/AKT-associated signaling alterations, accompanied by changes in CD86/CD206-associated brain myeloid phenotypic responses. These findings support AS-IV as a potential neuroimmunomodulatory intervention for ischemic stroke.</p> 2026-10-01T04:32:06Z Dataset Dataset 10.3389/fimmu.2026.1939189.s001 https://figshare.com/articles/dataset/Data_Sheet_1_Astragaloside_IV_attenuates_post-ischemic_neuroinflammation_associated_with_Treg-related_regulation_of_CD86_CD206-associated_brain_myeloid_phenotypic_responses_and_PI3K_AKT_signaling_alterations_zip/34038216 CC BY 4.0