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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.
Diabetic Kidney disease (DKD) is major complication of diabetes, and a leading cause of end stage renal disease, characterized by increased albuminuria, reduced estimated glomerular filtration rate, renal inflammation, fibrosis and functional decline. The Sonic Hedgehog (Shh) pathway has emerged as a critical regulator of extracellular matrix (ECM) accumulation causing fibrosis, inflammation in DKD. Natural products such as flavonoids are known to slow the progression of DKD which is already proven by several preclinical studies. Kaempferol is one such polyphenol found in many plants shows a wide range of pharmacological activities. This study evaluated the protective effects of kaempferol-enriched fraction (KEF) form Camellia sinensis against DKD both in vitro and in vivo.
In vitro, high-glucose stimulated rat mesangial cells and NRK-52E epithelial cells were treated with fraction to assess Cell viability, ROS scavenging activity, mitochondrial membrane potential, and the expression of inflammatory (NF-κB), fibrotic (TGF-β1, α-SMA, collagen IV), and Shh pathway (Shh, Gli1) markers via qPCR. In vivo, DKD was induced in Sprague–Dawley rats by intraperitoneal streptozotocin, followed by eight weeks of KEF administration. Renal function was assessed by serum creatinine, BUN, and urinary albumin-to-creatinine ratio. Histological changes were evaluated by H&E, Periodic Acid Schiff’ and Picrosirius red staining. IHC staining and western blotting were executed to evaluate the protein expression associated with shh signalling pathway.
KEF treatment significantly reduced Shh and Gli1 expression, lowered ROS levels, improved mitochondrial membrane potential, and downregulated NF-κB, TGF-β1, α-SMA, and collagen IV in a dose-dependent manner, suggesting therapeutic potential for DKD. In vivo, KEF improved body weight, glycemic control, kidney function markers (serum creatinine, BUN, urine microalbumin), reduced lipid peroxidation, and enhanced endogenous antioxidant enzymes. It also alleviated histopathological alterations and ECM accumulation in the mesangial region while normalizing mRNA levels of Shh, Gli1, nephrin, desmin, NF-κB, and TGF-β1. Rats administered with KEF have lowered the shh pathway related proteins, inflammatory and fibrotic markers, validated by western blot analysis showed the downregulation of pathway targeted proteins.
In conclusion, the results indicate protective role of KEF against DKD via inhibiting Shh pathway and its downstream effector Gli-1, KEF thereby, reducing fibrosis, ECM deposition, and inflammation. Both in vitro and in vivo findings confirmed improved renal architecture and function, along with decreased inflammation and fibrosis. These results highlight kaempferol as a promising phytotherapeutic agent for the prevention and management of DKD, offering a multi-targeted strategy to counter hyperglycemia-driven renal injury and progression toward end-stage renal disease.
