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Volume10, Issue 12 (Suppl) J Proteomics Bioinform, an open access journal
ISSN: 0974-276X
Page 36
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World Biomarkers & Pharma Biotech 2017
December 07-09, 2017
December 07-09, 2017 | Madrid, Spain
&
20th International Conference on
PHARMACEUTICAL BIOTECHNOLOGY
9th WORLD BIOMARKERS CONGRESS
JOINT EVENT ON
Cucurbitacin B mitigates experimental autoimmune encephalomyelitis by inhibition of IL-17/IL-23
immune axis
Nima Sanadgol
University of Zabol, Iran
Pharmacological approaches to inhibit brain acute inflammation may represent important strategies for the control of
autoimmune diseases. Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating and autoimmune disease of
the central nervous system (CNS). Cucurbitacin B (CuB), an oxygenated tetracyclic triterpenoid compound extracted from
Cucurbitaceae plant species, is a bioactive agent by disruption of microtubule polymerization and inhibition of JAK/STAT
signaling. However, there has been little information about impact of CuB on MS treatment. In this research, for the first time
we examine effects of CuB (specific STAT3 blocker), in experimental autoimmune encephalomyelitis (EAE) mouse model of
MS. EAE was induced by subcutaneous immunization of MOG35-55 in 8-week-old C57BL/6 mice. CuB was administered at
different doses (0.25, 0.5 and 1 mg/kg body weight/day/i.p) from the first day of the experiment. Inflammatory responses were
examined using qRT-PCR, western blot and immunohistochemistry (IHC) analysis of specific markers such as p-STAT3, IL-
17A, IL-23A, CD11b and CD45. CuB reduced STAT3 activation, leukocyte trafficking, and also IL-17/IL-23 immune axis in
this model. Treated mice with lower doses of CuB exhibited a considerable depletion in the EAE clinical score which correlated
with decreased expression of IL-17, IL-23 and infiltration of CD11b+ and CD45+ cells into the CNS. Our in vivo results suggest
that STAT3 inhibition by CuB will be an effective and new approach for the treatment of neuro-inflammatory disease such as
MS.
Recent Publications:
1. Doan V, Kleindienst A M, McMahon E J, Long B R, Matsushima G K and Taylor L C (2013) Abbreviated exposure to
cuprizone is sufficient to induce demyelination and oligodendrocyte loss. J Neurosci Res. 91: 363-73.
2. Kastelein R A, Hunter C A and Cua D J (2007) Discovery and biology of IL-23 and IL-27: related but functionally
distinct regulators of inflammation. Annu. Rev. Immunol. 25: 221-242.
3. Haines C J et al (2013) Autoimmune memory T helper 17 cell function and expansion are dependent on interleukin-23.
Cell Rep. 3: 1378-1388.
4. Ramroodi N, Khani M, Ganjali Z, Javan M R, Sanadgol N, Khalseh R and Abdollahi M (2015) Prophylactic effect of
BIO-1211 small-molecule antagonist of VLA-4 in the EAE mouse model of MS. Immunological Investigations. 44:
694-712.
Biography
Nima Sanadgol is expert in field of Cell and Molecular Neurobiology. His recent research emphasis is in treatment of neurodegenerative disease with use of new
natural compounds. He has particular interest in evaluation of mechanisms of neuron-glia interactions, in order to fascinating myelin repair and control of neuro-
inflammatory and neuro-degenerative diseases (Multiple sclerosis, Alzheimer, Parkinson, etc.). He has already gained so much experience in neuro-immune and
circuit-specific signaling in glial-neuron networks (T cell biology, NF-κB, Nrf2, MAP kinase, AMP kinase, apoptosis and autophagy).
Nima Sanadgol, J Proteomics Bioinform 2017, 10:12(Suppl)
DOI: 10.4172/0974-276X-C1-109