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Please use this identifier to cite or link to this item:
https://ir.csmu.edu.tw:8080/ir/handle/310902500/11645
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Title: | Cystamine ameliorates ventricular hypertrophy associated with modulation of IL-6-mediated signaling in lupus-prone mice. |
Authors: | Tzang, BS Hsu, TC Chen, TY Huang, CY Li, SL Kao, SH |
Contributors: | 中山醫學大學 |
Keywords: | Cystamine;Lupus-prone mice;Left ventricular hypertrophy;IL-6;MEK5 |
Date: | 2013 |
Issue Date: | 2015-07-27T08:13:47Z (UTC)
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ISSN: | 0024-3205 |
Abstract: | AIMS:
The aim of this study is to investigate the protective effects of cystamine on lupus-associated cardiac hypertrophy.
MAIN METHODS:
Balb/c and lupus-prone NZB/W-F1 mice were individually randomized into sham group (saline, n=16) and cystamine group (n=16). Mice received saline or cystamine (100 mmol in 100 μL saline) by daily intraperitoneal injection for 2 consecutive weeks. Morphological, histological, and biochemical alterations were investigated.
KEY FINDINGS:
Cystamine decreased both left ventricular (LV) mass and LV mass/tissue-to-blood ratio (TBR) in NZB/W-F1 mice (p<0.05), whereas slight effects were observed in Balb/c mice. Moreover, cystamine reduced levels of atrial natriuretic peptide (ANP), C-reactive protein (CRP), heart type-fatty acid binding protein (h-FABP), creatine kinase-MB (CK-MB) and IL-6 in LV tissues of NZB/W-F1 mice (p<0.05). Additionally, in LV tissues of NZB/W-F1 mice, suppression of hypertrophic signaling mediated by IL-6 in response to administration of cystamine was revealed, including phosphorylation of MEK5, ERK5, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) (p<0.05).
SIGNIFICANCE:
Cystamine alleviated LV hypertrophy in NZB/W-F1 mice as a result of decrease in hypertrophic mediators and suppression of IL-6 mediated hypertrophic signaling.
Copyright © 2013 Elsevier Inc. All rights reserved. |
URI: | https://ir.csmu.edu.tw:8080/ir/handle/310902500/11645 http://dx.doi.org/10.1016/j.lfs.2013.01.027 |
Relation: | Life Sci. 2013 Apr 9;92(12):719-26. |
Appears in Collections: | [免疫學研究所] 期刊論文
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