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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Cisplatin(cis-diamminedichloroplatinum II, CDDP), a widely used chemotherapeutic agent, is clinically limited by nephrotoxicity. Acetyl-11-keto-β-boswellic acid (AKBA), an active triterpenoid compound from the extract of Olibanum, shows nephroprotective potential. This study investigated AKBA's protective effects and mechanisms in CDDP-induced acute kidney injury (AKI).
Network pharmacology identified active components and target genes of Olibanum. Bioinformatics analysis screened differentially expressed genes and conducted functional enrichment (GO/KEGG). Molecular docking and molecular dynamic (MD) simulations confirmed AKBA's binding to target proteins. CDDP-induced AKI mouse models and human proximal tubular epithelial cells (HK2) injury models were established to reveal AKBA's nephroprotective mechanisms. Lewis lung carcinoma (LLC) tumor-bearing mice and human A549 lung cancer cells further validated AKBA's compatibility with CDDP antitumor efficacy.
Network pharmacology revealed 8 bioactive components and 193 potential targets of Olibanum, with AKBA as the core component interacting with 56 cross-validated targets. Protein-protein interaction (PPI) network analysis prioritized 18 hub genes functionally enriched in oxidative stress (GO) and ferroptosis/apoptotic pathways (KEGG). Molecular docking and MD simulations demonstrated AKBA's robust binding stability with PTGS2, P53, GPX4 and PPARγ, indicating multi-target modulation. In vivo, AKBA attenuated CDDP-induced AKI by reducing plasma creatinine, renal KIM-1/NGAL expression, and suppressing tubular Oxidative Stress and ferroptosis. In vitro, AKBA alleviates cisplatin-induced renal tubular epithelial cell ferroptosis through ROS/HO-1/GPX4 axis. Notably, AKBA preserved CDDP's tumor-suppressive effects in both LLC-bearing mice and A549 cells.
AKBA protects against CDDP-induced AKI by inhibiting oxidative stress and ferroptosis through targeting the P53/Nrf2/GPX4 pathway, without compromising CDDP's antitumor activity. These findings highlight AKBA as a promising adjunctive therapy for CDDP-associated nephrotoxicity.
