BOR-SHOW TZANGTSAI-CHING HSUSHAO-HSUAN KAO2026-10-162026-10-162013-04-09Pure ID: 15330205Pure UUID: ad584bb9-85f1-47c2-b2ef-836df1b621be10.1016/j.lfs.2013.01.027https://www.scopus.com/pages/publications/84875224282https://scholars.csmu.edu.tw/handle/123456789/23401Aims 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.8enjournal article