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Geniposide protects pancreatic INS‐1E β cells from hIAPP‐induced cell damage: Potential involvement of insulin degrading‐enzyme
Author(s) -
Zhang Yonglan,
Yin Fei,
Liu Jianhui,
Wang Yanwen
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10394
Subject(s) - amylin , islet , cytotoxicity , amyloid (mycology) , chemistry , insulin degrading enzyme , downregulation and upregulation , insulin , enzyme , pancreatic islets , peptide , cell , biochemistry , microbiology and biotechnology , endocrinology , in vitro , biology , inorganic chemistry , gene
Islet amyloid deposition is increasingly seen as a pathogenic feature of type 2 diabetes mellitus (T2DM), with the deposits containing the unique amyloidogenic peptide islet amyloid polypeptide (IAPP, also known as amylin). The fibril precursors of IAPP contribute to its cytotoxicity on pancreatic β cells and be important in causing β‐cell dysfunction in T2DM. However, the development of effective this study, inhibitors against the toxicity of IAPP has been extremely challenging. We have found that pre‐incubation with geniposide dose‐dependently prevented human IAPP (hIAPP)‐induced cell damage in INS‐1E cells, and bacitracin, an inhibitor of IDE activity, prevented significantly the protective effects of geniposide in pancreatic INS‐1E cells significantly. Geniposide induced the expression of insulin‐degrading enzyme (IDE), a key degrading protein of hIAPP, but had no significant effect on the aggregation of hIAPP. These findings indicate that geniposide prevents hIAPP‐induced cytotoxicity in INS‐1E cells involving upregulation of IDE expression.