Cited 0 times in

60 2

Lithospermic acid B protects β-cells from cytokine-induced apoptosis by alleviating apoptotic pathways and activating anti-apoptotic pathways of Nrf2-HO-1 and Sirt1.

Authors
 Byung-Wan Lee ; Sung Wan Chun ; Hyun Chul Lee ; Bong-Soo Cha ; Eun Seok Kang ; Yongho Lee ; Soo Hyun Kim 
Citation
 Toxicology and Applied Pharmacology, Vol.252(1) : 47~54, 2011 
Journal Title
 Toxicology and Applied Pharmacology 
ISSN
 0041-008X 
Issue Date
2011
Abstract
Lithospermic acid B (LAB) has been reported to protect OLETF rats, an established type 2 diabetic animal model, from the development of diabetes-related vascular complications. We investigated whether magnesium lithospermate B (LAB) has a protective role under cytokine-induced apoptosis in INS-1 cells in vitro and whether it slows the development of diabetes in OLETF rats in vivo. Pretreatment with 50 μM LAB significantly reduced the 1000 U/mL INF-γ and 100 U/mL IL-1β-induced INS-1 cell death. LAB significantly alleviated cytokine-induced phosphorylations of p38 and JNK in accordance with a decrease in cleaved caspase-3 activity in beta-cells. LAB also protected against the cytokine-induced caspase-3 apoptotic pathway via significant activation of Nrf2-HO (heme-oxygenase)-1 and Sirt1 expression. OLETF rats treated with 40 mg/kg/day LAB showed a significant improvement in glucose tolerance compared to untreated OLETF control rats in vivo. Our results suggest that the cytoprotective effects of LAB on pancreatic β-cells are related with both alleviating apoptotic pathways and activating anti-apoptotic pathways of Nrf2-HO-1 and Sirt1.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/94144
DOI
10.1016/j.taap.2011.01.018
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
Yonsei Authors
사서에게 알리기
  feedback
Link
 http://www.sciencedirect.com/science/article/pii/S0041008X11000354
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse