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Your search keyword '"Hattori, Shunji"' showing total 15 results
Start Over Author "Hattori, Shunji" Publisher wiley
15 results on '"Hattori, Shunji"'

3. Silibinin protects rat pancreatic β‐cell through up‐regulation of estrogen receptors' signaling against amylin‐ or Aβ1–42‐induced reactive oxygen species/reactive nitrogen species generation

Author

Yang, Jing, primary, Sun, Yue, additional, Xu, Fanxing, additional, Liu, Weiwei, additional, Hayashi, Toshihiko, additional, Hattori, Shunji, additional, Ushiki‐Kaku, Yuko, additional, Onodera, Satoshi, additional, Tashiro, Shin‐ichi, additional, and Ikejima, Takashi, additional

Published
2019
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8. Acceleration of bone formation during fracture healing by injectable collagen powder and human basic fibroblast growth factor containing a collagen-binding domain fromClostridium histolyticumcollagenase

Author

Saito, Wataru, primary, Uchida, Kentaro, additional, Ueno, Masaki, additional, Matsushita, Osamu, additional, Inoue, Gen, additional, Nishi, Nozomu, additional, Ogura, Takayuki, additional, Hattori, Shunji, additional, Fujimaki, Hisako, additional, Tanaka, Keisuke, additional, and Takaso, Masashi, additional

Published
2013
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15. Silibinin protects rat pancreatic β-cell through up-regulation of estrogen receptors' signaling against amylin- or Aβ 1-42 -induced reactive oxygen species/reactive nitrogen species generation.

Author

Yang J, Sun Y, Xu F, Liu W, Hayashi T, Hattori S, Ushiki-Kaku Y, Onodera S, Tashiro SI, and Ikejima T

Subjects
Animals, Antioxidants pharmacology, Apoptosis drug effects, Cells, Cultured, Cytoprotection drug effects, Down-Regulation drug effects, Insulin-Secreting Cells metabolism, Rats, Reactive Nitrogen Species metabolism, Reactive Oxygen Species metabolism, Receptors, Estrogen drug effects, Signal Transduction drug effects, Up-Regulation drug effects, Amyloid beta-Peptides toxicity, Insulin-Secreting Cells drug effects, Islet Amyloid Polypeptide toxicity, Peptide Fragments toxicity, Protective Agents pharmacology, Receptors, Estrogen metabolism, Silybin pharmacology
Abstract

Amylin and amyloid-β (Aβ) were found to induce reactive oxygen species (ROS) and reactive nitrogen species (RNS) in rat pancreatic β-cell line, INS-1 cells, leading to cell death. In this study, we report on reciprocal relationship between the expression of estrogen receptors (ERs) α and β (ERα and ERβ) and generation of ROS/RNS in amylin/Aβ 1-42 -treated INS-1 cells. That is, pharmacological activation of ERs in INS-1 cells significantly decreases ROS/RNS generation, but blockage of ERs increases ROS/RNS generation. Silibinin is a natural polyphenolic flavonoid isolated from milk thistle with phytoestrogen activities, also known as silybin. Treatment with silibinin down-regulated ROS/RNS production induced by treatment with amylin/Aβ 1-42 in the cells. Silencing ERs expression with siRNAs targeting ERs showed that the protective effect of silibinin was markedly weakened, indicating that silibinin protection is largely attributed to activation of ERs' signaling. The binding of silibinin to ERs implies that the protective effect of silibinin on amylin/Aβ 1-42 -treated INS-1 cells owes to down-regulation of ROS/RNS through the activation of ERs phosphorylation. Amylin and Aβ 1-42 cotreatment enhanced furthermore ROS/RNS generation and cytotoxicity through further down-regulation of ERs phosphorylation, and this was reversed by silibinin. Silibinin also protects INS-1 cells from amylin and Aβ 1-42 cotreatment. These results indicate that protective effect of silibinin is mediated by enhancement of ERs phosphorylation that depresses ROS/RNS generation in amylin/Aβ 1-42 -treated INS-1 cells., (© 2019 John Wiley & Sons, Ltd.)

Published
2019
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