Nanocurcumin is a potential novel therapy for multiple sclerosis by influencing inflammatory mediators

Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Inflammation has ever been thought as disadvantageous in the pathophysiology of MS. Nanocurcumin has been used as an anti-inflammatory compound. The aim of this study was to identify effects of nanocurcumin on inflammatory mediators in patients with relapsing-remitting multiple sclerosis (RRMS). Methods: Fifty MS patients were randomly divided into two groups. The test group received nanocurcumin capsule daily for 6 months. Simultaneously, the control group received placebo. Real-Time PCR was employed to detect the probable changes in gene expression levels of miRNAs, and miRNA-dependent targets, and also transcription factors and pro-inflammatory cytokines in blood samples. ELISA was used to determine the alterations in these cytokines secretion levels. We have also examined EDSS score in MS patients in two groups. Results: According to the results, a significant decrease in mRNA expression levels of miR-145 (p < 0.0001), miR-132 (p = 0.004), miR-16 (p = 0.0034), STAT1 (p = 0.0002), NF-kappa B (p < 0.0001), AP-1 (p = 0.0007), IL-1 beta (p = 0.0017), IL-6 (p = 0.017), IFN-gamma (p < 0.0001), CCL2 (p = 0.0067), CCL5 (p = 0.0034), TNF-alpha (p < 0.0001) and also significant increase in expression levels of miRNAs targets; Sox2 (p = 0.0001), sirtuin-1(p = 0.0007), Foxp3 (p = 0.0082), PDCD1 (p = 0.003) was evident in nanocurcumin treated group compared with before treatment. The secretion levels of IFN-gamma (p = 0.0025), CCL2 (p = 0.0029), and CCL5 (p = 0.0003) were reduced dramatically in test group compared with placebo group. Conclusion: In conclusion, nanocurcumin may be more effective on the inflammatory features of MS. According to present results, nanocurcumin may inhibit neuroinflammation in MS patients. (c) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.