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.

Highlights

  • Systemic lupus erythematosus (SLE) is an autoimmune disorder that only affects women

  • Left ventricular weight (LVW) and the proportions of entire heart weight to tibia length (WHW/Tibia) and left ventricular weight to tibia length (LVW/Tibia) in the GMNL-32 groups did not show much difference when compared to the SLE control group (Table 1)

  • Our results reveal that there was a significant increase in body weight in NZB/W F1 mice groups treated with GMNL-32 there was no significant change observed in the heart weight or the left ventricle weight

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Summary

Introduction

Systemic lupus erythematosus (SLE) is an autoimmune disorder that only affects women. It has been reported that women of 44–50 years of age have a 50-fold increased risk of myocardial infarction [5]. In SLE patients apoptosis has been firmly related with different autoantibodies such as anti-phospholipids and anti-oxidized low-density lipoprotein antibodies and the engagement of these autoantibodies with self-tissue is considered to enact the supplement framework, cell-interceded cytotoxicity, and cardiomyocyte apoptosis [10,11]. For this reason, restraint of cardiovascular apoptosis is recommended to improve autoantibody-incited heart injuries in SLE patients

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