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Quercetin is a dietary flavonoid that shows effective neuroprotective action in cellular and animal models of Alzheimer's disease and Huntington's disease. However, its therapeutic application is limited due to low water solubility and cytotoxicity at the working concentration in the 20-100 μM range. Here we report a nanoparticle form of quercetin (nanoquercetin) that shows antiamyloidogenic performance at lower quercetin concentration (one micromolar) and inhibits polyglutamine (mutant huntingtin) aggregation in Huntington's disease cell model. Nanoquercetin is composed of a polyaspartic acid-based polymer micelle encapsulated with quercetin (3-5 wt %) and colloidal in nature with <100 nm hydrodynamic size. It enters into the cell via endocytosis and slowly releases molecular quercetin in a >3 day time scale that offers better antiamyloidogenic performance via up-regulated autophagy processes. This work shows that nanoformulation of antiamyloidogenic molecule can have better performance as compared to respective molecule.
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http://dx.doi.org/10.1021/acsabm.9b00518 | DOI Listing |
Trends Biochem Sci
September 2025
Department of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, USA. Electronic address:
Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene, resulting in an expanded polyglutamine (polyQ) tract in HTT protein. Expanded polyQ tracts cause mutant HTT (mHTT) to aggregate and accumulate as cellular inclusions. Recent studies highlight the interactions between mHTT and different cellular membranes that contribute to HD pathogenesis.
View Article and Find Full Text PDFEur J Gastroenterol Hepatol
September 2025
Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, The University of Jordan, Jordan University Hospital.
Aim: The purpose of our study was to evaluate the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and its associated risk factors in patients with inflammatory bowel disease (IBD).
Methods: This was a retrospective chart review of patients who underwent treatment for IBD at Jordan University Hospital between January 2013 and 2022. Case finding methods and clinical chart reviews were used to evaluate the clinical profile of patients with IBD.
PLoS One
September 2025
Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology & Immunology, Medical University of Vienna, Vienna, Austria.
Advanced glycation end products (AGEs) and reactive intermediates, such as methylglyoxal, are formed during thermal processing of foods and have been implicated in the pathogenesis of a series of chronic inflammatory diseases. AGEs are thought to directly interact with the intestinal epithelium upon ingestion of thermally processed foods, but their effects on intestinal epithelial cells are poorly understood. This study investigated transcriptomic changes in human intestinal epithelial FHs 74 Int cells after exposure to AGE-modified human serum proteins (AGE-HS), S100A12, a known RAGE ligand, and unmodified human serum proteins (HS).
View Article and Find Full Text PDFInflammopharmacology
September 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA University), Giza, Egypt.
The neuroprotective potential of tyrosine kinase inhibitors (TKIs), potent anticancer drugs, was verified against various neurodegenerative insults, but not Huntington's disease (HD). These promising outcomes were due to their ability to modulate various intracellular signalling pathways. Hence, the current study aimed to evaluate the neuroprotective effects of lapatinib and pazopanib in the 3-nitropropionic (3-NP)-induced HD model in rats.
View Article and Find Full Text PDFRSC Med Chem
August 2025
Department of Biological Science, Birla Institute of Technology and Science, Pilani Hyderabad Campus, Jawahar Nagar, Kapra Mandal, Medchal District Telangana 500078 India
Mitochondrial dysfunction is one of the primary cellular conditions involved in developing Huntington's disease (HD) pathophysiology. The accumulation of mutant huntingtin protein with abnormal PolyQ repeats resulted in the death of striatal neurons with enhanced mitochondrial fragmentation. In search of neuroprotective molecules against HD conditions, we synthesized a set of isoxazole-based small molecules to screen their suitability as beneficial chemicals improving mitochondrial health.
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