Hu Wei-Syun, Rajendran Peramaiyan, Tzang Bor-Show, Yeh Yu-Lan, Shen Chia-Yao, Chen Ray-Jade, Ho Tsung-Jung, Vijaya Padma Viswanadha, Chen Yi-Hsing, Huang Chih-Yang
School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan, ROC.
Division of Cardiovascular Medicine, Department of Medicine, China Medical University Hospital, Taichung, Taiwan, ROC.
PLoS One. 2017 Sep 21;12(9):e0185098. doi: 10.1371/journal.pone.0185098. eCollection 2017.
Systemic lupus erythematosus (SLE) is a disease that mostly affects women. Accelerated atherosclerosis is a high-risk factor associated with SLE patients. SLE associated with cardiovascular disease is one of the most important causes of death. In this study, we demonstrated that Lactobacillus paracasei GMNL-32 (GMNL-32), a probiotic species, exhibits anti-fibrosis and anti-apoptotic effects on the cardiac tissue of NZB/WF1 mice. Female NZB/W F1 mice, a well-known and commonly used lupus-prone mouse strain, were treated with or without GMNL-32 administration for 12 weeks. Oral administration of GMNL-32 to NZB/WF1 mice significantly increased the ventricular thickness when compared to that of NZB/WF1 mice. Administration of GMNL-32 significantly attenuated the cardiac cell apoptosis that was observed in exacerbate levels in the control NZB/WF1 mice. Further, the cellular morphology that was slightly distorted in the NZB/WF1 was effectively alleviated in the treatment group mice. In addition, GMNL-32 reduced the level of Fas death receptor-related pathway of apoptosis signaling and enhanced anti-apoptotic proteins. These results indicate that GMNL-32 exhibit an effective protective effect on cardiac cells of SLE mice. Thus, GMNL-32 may be a potential therapeutic strategy against SLE associated arthrosclerosis.
系统性红斑狼疮(SLE)是一种主要影响女性的疾病。动脉粥样硬化加速是与SLE患者相关的高危因素。SLE相关的心血管疾病是最重要的死亡原因之一。在本研究中,我们证明了副干酪乳杆菌GMNL-32(GMNL-32),一种益生菌,对NZB/WF1小鼠的心脏组织具有抗纤维化和抗凋亡作用。雌性NZB/W F1小鼠是一种著名且常用的狼疮易感小鼠品系,接受或不接受GMNL-32处理12周。与NZB/WF1小鼠相比,给NZB/WF1小鼠口服GMNL-32显著增加了心室厚度。给予GMNL-32显著减轻了在对照NZB/WF1小鼠中观察到的加剧水平的心肌细胞凋亡。此外,在NZB/WF1中略有扭曲的细胞形态在治疗组小鼠中得到有效缓解。此外,GMNL-32降低了Fas死亡受体相关的凋亡信号通路水平并增强了抗凋亡蛋白。这些结果表明GMNL-32对SLE小鼠的心肌细胞具有有效的保护作用。因此,GMNL-32可能是一种针对SLE相关动脉粥样硬化的潜在治疗策略。