<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE302nnn/GSE302127/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE302127</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Galaxamide improve cisplatin-induced uterine damage via attenuating inflammation and apoptosis in in mice</name><description>Objective: To evaluate the protective effects of marine cyclopeptide galaxamide against cisplatin-induced uterine toxicity in cervical cancer models, focusing on macrophage polarization and NF-κB signaling modulation ​Methods: In vivo tumor-bearing mouse models and in vitro cervical cancer cell lines were treated with cisplatin (CIS, 5 mg/kg) ± galaxamide (20 mg/kg). Uterine histopathology (hematoxylin-eosin staining), apoptosis (TUNEL assay), macrophage subsets (flow cytometry for M1/M2 markers), NF-κB activation (western blot for p65 phosphorylation), and serum cytokines (ELISA for TNF-α/IL-6) were analyzed. Embryo implantation rates were assessed to quantify endometrial receptivity ​Results: Cisplatin caused significant endometrial atrophy (↓45% thickness vs. control, P&lt;0.01), NF-κB hyperactivation (2.8-fold p65 increase), and M1-macrophage dominance (M1/M2 ratio ↑40%). These changes correlated with elevated pro-inflammatory cytokines (TNF-α↑300%, IL-6↑180%) and reduced embryo implantation (↓67%, P&lt;0.001). Galaxamide co-treatment: Suppressed NF-κB activation (p65↓65%, P&lt;0.01) and apoptosis (TUNEL+ cells↓50%) Restored M2-macrophages (↑25%, P&lt;0.05) and cytokine balance (TNF-α↓55%, IL-6↓48%) Preserved endometrial integrity and increased implantation rates (1.9-fold vs. CIS alone, P&lt;0.01) ​Conclusion: Galaxamide mitigates cisplatin-induced uterine damage by reprogramming macrophages toward M2 phenotype and inhibiting NF-κB-mediated inflammation, offering a promising adjuvant strategy to preserve fertility in young cervical cancer patients ​Keywords: cisplatin toxicity, uterine protection, galaxamide, macrophage polarization, NF-κB pathway</description><dates><publication>2026/09/01</publication></dates><accession>GSE302127</accession><cross_references><GSM>GSM9096721</GSM><GSM>GSM9096720</GSM><GSM>GSM9096723</GSM><GSM>GSM9096722</GSM><GSM>GSM9096725</GSM><GSM>GSM9096724</GSM><GSM>GSM9096718</GSM><GSM>GSM9096717</GSM><GSM>GSM9096719</GSM><GPL>28430</GPL><GSE>302127</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>