期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 97, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2021.107715
关键词
Silymarin; Multiple sclerosis; Interferon beta; Th 1; Th17; Treg; ALT; AST
资金
- Student research committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran [195012]
The study demonstrates that simultaneous treatment of multiple sclerosis patients with Silymarin and IFN-beta can significantly reduce liver enzyme levels, decrease the percentage of Th17 cells, increase the frequency of Treg cells, lower IL-17 and IFN gamma levels, and raise IL-10 and TGF beta levels.
Interferon beta (IFN-beta) has successfully been experimented with to treat multiple sclerosis (MS). However, patients sometimes do not respond effectively to treatment, and adverse effects, including liver toxicity, accompany this therapy. Accordingly, we decided to treat MS patients simultaneously with Silymarin (SM) as an immunomodulatory and hepatoprotective agent and IFN-beta in a clinical trial study. Complete blood count (CBC), liver enzyme levels, and the serum concentration of inflammatory and antiinflammatory cytokines were measured. Also, the frequency of immune cells was determined by flow cytometry. Liver enzyme levels were significantly lower in the intervention group (p < 0.05). The percentage of Th17 cells in the intervention group was significantly reduced compared to the placebo group (P < 0.001). Also, the frequency of Treg cells after treatment with SM plus IFN-beta was significantly increased compared to the placebo group (p < 0.05). Furthermore, the IL-17 and IFN gamma cytokine levels were significantly reduced in the intervention group (p < 0.05). Moreover, the levels of anti-inflammatory cytokines IL-10 and TGF beta were significantly increased in the intervention group (P < 0.05). Overall, the results provide novel and supplementary information on SM's notable immunoregulatory effects on inflammatory response and liver function in MS patients. Clinical Trial Identifier Number: IRCTID: IRCT20171220037977N1.
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