Tetramethylpyrazine ameliorates experimental autoimmune encephalomyelitis by modulating the inflammatory response
- Department of Histology and Embryology, Binzhou Medical University, Yantai (China)
- Department of Critical Care Medicine, Yu Huang Ding Hospital, Qingdao University, Yantai (China)
- Department of Pathology, Binzhou Medical University, Yantai (China)
Highlights: • TMP improves clinical scores in EAE mice. • TMP decreases demyelination in EAE mice. • TMP reduces inflammatory infiltration and glial activation in EAE mice. • TMP reduces NLRP3 inflammasome expression and modulates the Th1/Th17/Th2 response. Multiple sclerosis (MS) is a disabling inflammatory and demyelinating disorder of the central nervous system. Tetramethylpyrazine (TMP) has been demonstrated to ameliorate cerebral ischemic injury and spinal cord injury by inhibiting inflammatory cell activation and pro-inflammatory cytokine production. However, the effects of TMP on MS have not been studied. In this study, we evaluated the effects of TMP on the inflammatory response in experimental autoimmune encephalomyelitis (EAE), which is an animal model of MS. TMP (30 mg/kg) treatment significantly reduced the expression levels of NLR Family, Pyrin Domain-Containing 3 Protein inflammasome and caspase-1and decreased inflammatory infiltration and glial activation. Moreover, TMP (30 mg/kg) suppressed the expression of pro-inflammatory cytokines (interleukin-18 [IL-18] and IL-17) and promoted the expression of an anti-inflammatory cytokine (IL-10). The reduced inflammatory response resulted in improvement in clinical scores and decreased demyelination in EAE mice. Therefore, our results demonstrate that TMP (30 mg/kg) improved functional recovery in part by reducing inflammation in EAE mice. TMP may be a potential therapeutic agent for MS therapy.
- OSTI ID:
- 23134319
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 503, Issue 3; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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