期刊
SCIENTIFIC REPORTS
卷 8, 期 -, 页码 -出版社
NATURE RESEARCH
DOI: 10.1038/s41598-017-18807-8
关键词
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资金
- German Federal Ministry of Education and Research [01KX1012]
- German Center for Diabetes Research (DZD e.V.)
- Deutsche Forschungsgemeinschaft, DFG [SFB-1035]
- Helmholtz-Gemeinschaft
- DFG [Re1435]
- Center for Integrated Protein Science Munich (CIPS-M)
- GO-Bio Initiative of the German Federal Ministry for Education and Research (BMBF) [0313881]
- ERA-NET NEURON initiative
- BMBF [01W1301]
- Berlin Institute of Health Collaborative Research Grant [1.1.2.a.3]
- BMBF
- Helmholtz Validation Fund [HVF-0013]
- Helmholtz Association, Germany
- Max Delbruck Center for Molecular Medicine in the Helmholtz Association
The formation of amyloid fibrils by human islet amyloid polypeptide protein (hIAPP) has been implicated in pancreas dysfunction and diabetes. However, efficient treatment options to reduce amyloid fibrils in vivo are still lacking. Therefore, we tested the effect of epigallocatechin gallate (EGCG) on fibril formation in vitro and in vivo. To determine the binding of hIAPP and EGCG, in vitro interaction studies were performed. To inhibit amyloid plaque formation in vivo, homozygous (tg/tg), hemizygous (wt/tg), and control mice (wt/wt) were treated with EGCG. EGCG bound to hIAPP in vitro and induced formation of amorphous aggregates instead of amyloid fibrils. Amyloid fibrils were detected in the pancreatic islets of tg/tg mice, which was associated with disrupted islet structure and diabetes. Although pancreatic amyloid fibrils could be detected in wt/tg mice, these animals were non-diabetic. EGCG application decreased amyloid fibril intensity in wt/tg mice, however it was ineffective in tg/tg animals. Our data indicate that EGCG inhibits amyloid fibril formation in vitro and reduces fibril intensity in non-diabetic wt/tg mice. These results demonstrate a possible in vivo effectiveness of EGCG on amyloid formation and suggest an early therapeutical application.
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