Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Podocytes are considered the crucial cells involved in the progression of multiple glomerular diseases, and their damage can directly lead to proteinuria. Yiqi Qingre Gao (YQQRG), a formula of Chinese herbal medicine, has shown therapeutic effects on glomerular diseases. However, the underlying mechanisms remain obscure. The interaction between autophagy and NLRP3 inflammasome appears to be a potentially protective mechanism for podocytes.
An adriamycin (ADR)-induced mouse model of renal injury and a model of MPC-5 cell damage were employed, followed by intervention with YQQRG. Overexpression plasmid NLRP3 as well as the autophagic inhibitor 3-MA were used for further mechanistic studies. The location of autophagy and NLRP3 in podocytes was observed using immunofluorescence co-localization. The dynamic processes of autophagosome formation and degradation in podocytes were monitored using mCherry-eGFP-LC3 adenovirus. Other results were assessed by transmission electron microscopy, immunofluorescence staining, and western blotting.
Treatment of YQQRG significantly improved albuminuria, renal function and pathological damage in ADR-induced mice. Glomerular autophagic blockage and NLRP3 inflammasome activation following ADR intervention, specifically in podocytes, were ameliorated by YQQRG. Our results showed that YQQRG treatment diminished expression of NRLP3-related proteins cle-caspase1, IL-1βand IL18, and reduced inflammatory factors in the serum of ADR-induced mice, accompanied by improved autophagosome accumulation in podocytes and decreased autophagic biomarkers LC3 and P62. Consistent with in vivo results, YQQRG prevented apoptosis of podocytes exposed to ADR, and exhibited the effect of autophagy promotion and NLRP3 inhibition. We found that the number of autophagosomes labeled with yellow signal in podocytes was markedly enhanced, and the number of autolysosomes labeled with free red signal was reduced in response to ADR treatment. Both signals were improved by YQQRG co-incubation, indicating restoration of autophagic flux. Moreover, the addition of an overexpression plasmid NLRP3 and an autophagic inhibitor 3-MA attenuated the protective effect of YQQRG in ADR-stimulated MPC5 cells.
These findings indicate YQQRG protects podocytes via regulating the crosstalk between autophagy and NLRP3 inflammasome. Thus, YQQRG may be a therapeutic candidate for glomerular diseases.
