| Autor: |
Park, Jun Hong, Nam, YoonYi, Park, So-Young, Kim, Jin-Kyung, Choe, Nong-Hoon, Lee, Jae-Young, Oh, Yang-Seok, Suh, Jun Gyo |
| Zdroj: |
Journal of Biochemical & Molecular Toxicology; Jul2011, Vol. 25 Issue 4, p238-243, 6p |
| Abstrakt: |
High glucose levels induce cell death in many cell types, including pancreatic β-cells. Although protective agents against glucotoxicity have been searched for extensively, so far none have been found. In this report, we tested silk fibroin (SF) as a candidate material for antiglucotoxicity in the pancreatic β-cell (HIT-T15 cell) line. Approximately 50% of cells were killed after treatment with 80 mg/mL glucose. This reduction of cell number was recovered by the addition of SF at 50 mg/mL. SF treatment also decreased cellular reactive oxygen species (ROS) and increased proliferating cellular nuclear antigen (PCNA) immunoreactivity. In addition, TUNEL assays demonstrated that SF protects against glucose-induced apoptosis of HIT-T15 cells, suggesting that SF might protect cells from cell death by lowering cellular ROS levels. SF also induced expression of the insulin-like growth factor-1 (IGF-1) gene, and IGF-1 expression may be the cause of SF-induced protection against glucose toxicity. Taken together, these results suggest that SF could serve as a potential therapeutic agent to treat the hyperglycemia-induced death of pancreatic β-cells. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:238-243, 2011; View this article online at . DOI 10.1002/jbt.20381 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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