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PLoS One. 2017 Sep 21;12(9):e0185098. doi: 10.1371/journal.pone.0185098. eCollection 2017.

Lactobacillus paracasei GMNL-32 exerts a therapeutic effect on cardiac abnormalities in NZB/W F1 mice.

Author information

1
School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan, ROC.
2
Division of Cardiovascular Medicine, Department of Medicine, China Medical University Hospital, Taichung, Taiwan, ROC.
3
Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC.
4
Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan, ROC.
5
Department of pathology, Changhua Christian Hospital, Changhua, Taiwan, ROC.
6
Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan, ROC.
7
Department of Nursing, Mei Ho University, Pingtung, Taiwan, ROC.
8
Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, ROC.
9
Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan, ROC.
10
Department of Biotechnology, Bharathiar University, Coimbatore, India.
11
Research and Development Department, GenMont Biotech Incorporation, Tainan, Taiwan, ROC.
12
Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, ROC.

Abstract

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.

PMID:
28934296
PMCID:
PMC5608316
DOI:
10.1371/journal.pone.0185098
[Indexed for MEDLINE]
Free PMC Article

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