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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.
Recent studies have shown that tubular injury in diabetic kidney disease (DKD), known as diabetic tubulopathy (DT), is an independent pathogenic factor that occurs alongside glomerular and microvascular lesions and contributes to the progression of DKD. Fortunately, there are effective treatments specifically targeting DT with traditional Chinese medicine (TCM) in China. Therein Abelmoschus manihot (L.) Medik (AM) as a medicinal plant is widely reported to be used for the treatment of DT in China, and that its effects are different from sodium-glucose co-transporter 2 (SGLT2) inhibitors in vivo. Therefore, exploring new therapeutic strategies that combine AM with SGLT2 inhibitors has become one of the key topics in the field of “Chinese-West medical collaboration”. This study thereby aimed to clarify the therapeutic effects of the total flavones of Abelmoschus manihot (TFA), a natural extract derived from AM in combination with empagliflozin (EM), in comparison to EM alone, on renal dysfunction and tubular damage in DT, as well as the underlying therapeutic mechanisms.
For in vivo experiments, modified DT rat models were administered one of the following treatments: high-dose TFA+EM (H-TFA+EM), low-dose TFA+EM (L-TFA+EM), EM alone, or vehicle. For in vitro studies, NRK-52E cells were exposed to high-glucose, with or without H-TFA+EM, L-TFA+EM, EM, phosphatidylinositol 3-kinase knockdown lentivirus, rotenone, olaparib, Mdivi-1, or MitoQ. Compound target prediction for TFA+EM, molecular docking validation, and transcriptomic analysis were performed.
TFA+EM treatment improved renal dysfunction markers including blood glucose, urinary N-acetyl-β-D-glucosaminidase, serum creatinine, and blood urea nitrogen in a dose-dependent manner. The therapeutic efficacy of H-TFA+EM was superior to that of L-TFA+EM or EM alone. In vivo, H-TFA+EM effectively alleviated TIF, suppressed inflammatory factor expression, and mitigated oxidative stress (OS)-induced tubular injury in diabetic kidneys. Mechanistically, activation of the PI3K/Akt/mTOR signaling pathway was identified as a central target of TFA+EM’s action against DT. Further in vivo and in vitro analyses confirmed that the renoprotective effects of H-TFA+EM were closely associated with inhibition of the PI3K/Akt/mTOR signaling pathway activation and reduction of mitochondria-mediated oxeiptosis in tubular epithelial cells.
In this study, we demonstrated that TFA+EM, superior to EM alone, reduces renal disfunction and TIF in DT, and that underpinning therapeutic mechanisms are closely related to inhibiting the PI3K/Akt/mTOR signaling pathway activation and reducing mitochondria-related oxeiptosis in the diabetic kidneys. Our findings provide novel pharmacological evidence for the use of TFA+EM as a novel “Chinese-West medical collaboration” strategy in the treatment of DT.
