Abstract

BACKGROUND: A growing body of evidence suggests that systemic lupus erythematosus (SLE) may result in reversible cognitive dysfunction. Vitamin D is considered important for neurons. The therapeutic effect of vitamin D was evaluated in a rat model of SLE.

MATERIAL AND METHODS: There were 20 male MRL/lpr mice randomly divided into the SLE model group and the vitamin D group, in addition, 10 male C57BL 6J mice were used as the control (CON) group. Vitamin D was administered intraperitoneally (2 μg/kg) for 4 weeks. After 4 weeks of continuing intervention, we tested the cognitive function using the Morris water maze. The expression of vitamin D receptor (VDR), amyloid-β, caspase-3, and Bcl-2 were detected by western blot analysis.

RESULTS: In the present study, we observed that vitamin D treatment alleviated neurobehavioral deficits in the mice with SLE. At the molecular levels, administration of vitamin D activated the expression of VDR and reduced the number of dead cells in the CA1 region of the hippocampus as well as regulated caspase-3 and Bcl-2 expression.

CONCLUSIONS: In conclusion, our results indicated that vitamin D played a protective role by suppressing inflammatory cytokines, thereby ultimately inhibiting the progression of apoptosis in a mouse model of SLE. Vitamin D may be promising as a protective intervention in SLE with cognitive dysfunction, and more and more experiments are warranted for its clinical testing in the near future.

Keywords: Calcitriol, Cognition Disorders, Immune System Diseases, Lupus Erythematosus, Discoid, Amyloid beta-Peptides, cognitive dysfunction, Cytokines, Hippocampus, Inflammation Mediators, interferon-gamma, Interleukin-2, Lupus Erythematosus, Systemic, Mice, Inbred C57BL, Mice, Inbred MRL lpr, Proto-Oncogene Proteins c-bcl-2, Time Factors, Vitamin D