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Published on: May 22, 2018
Benzbromarone, Quercetin, and Folic Acid Inhibit Amylin Aggregation
Laura C López1,2, Olga Varea3,4, Susanna Navarro5
1Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Ciencias, Universidad de Zaragoza, Pedro Cerbuna 12, 50009 Zaragoza, Spain. lclopez@unizar.es.
Researchers screened drugs to find inhibitors of human amylin (hIAPP) aggregation, a hallmark of type II diabetes. Quercetin showed potential in slowing aggregation and protecting pancreatic cells from damage.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Human amylin (hIAPP) aggregation in pancreatic β-cells is linked to type II diabetes.
- Abnormal hIAPP levels and amyloid formation contribute to β-cell apoptosis.
- Mechanisms underlying hIAPP-induced β-cell death require further investigation.
Purpose of the Study:
- Identify approved drugs that inhibit hIAPP aggregation.
- Investigate the therapeutic potential of identified compounds for type II diabetes.
- Explore the role of hIAPP aggregation in β-cell damage.
Main Methods:
- Screening of approved drug libraries for hIAPP aggregation inhibitors.
- In vitro assays: Thioflavin T binding, turbidimetry, Transmission Electron Microscopy.
- Cell culture models using pancreatic insulinoma cells exposed to hIAPP.
Main Results:
- Benzbromarone, quercetin, and folic acid demonstrated inhibition of hIAPP fiber formation in vitro.
- Quercetin provided partial protection to cultured pancreatic cells against hIAPP-induced cytotoxicity.
- Quercetin's protective effect may involve modulation of hIAPP aggregation and reduction of oxidative damage.
Conclusions:
- Approved drugs can inhibit hIAPP aggregation, offering tools for research and potential therapeutics.
- Quercetin emerges as a promising compound for mitigating hIAPP-related β-cell damage.
- Further research into quercetin's mechanism could lead to novel strategies for type II diabetes treatment.
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