Ying Chen1, Zhaoqi Hu2, Rui Li3, Wei Qiu3, Xueqiang Hu3, Zhiming Zhou4. 1. Department of Neurology, Yijishan Hospital, The First Affiliated Hospital of Wannan Medical College, Wuhu, China, zsxkscy@sina.com. 2. Department of Orthopaedics, Traditional Chinese Medicine Hospital of Wuhu City, The Affiliated Hospital of Anhui University of Chinese Medicine, Wuhu, China. 3. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. 4. Department of Neurology, Yijishan Hospital, The First Affiliated Hospital of Wannan Medical College, Wuhu, China.
Abstract
INTRODUCTION: Multiple sclerosis (MS) is a complex demyelinating disease involving central nervous system (CNS). It is still a challenge to secure an effective therapeutic strategy against this disease. Carbenoxolone (CBX) is a derivative of glycyrrhetinic acid, which is widely used in brain research for its gap-junction inhibition effects. Many researchers have observed CBX-mediated suppression of CNS inflammation in their studies. OBJECTIVE: We want to further examine its anti-inflammation effects in CNS demyelinating disease like MS. METHODS: Thus, our study applied an experimental autoimmune encephalomyelitis (EAE) mouse model and examined the effects of CBX on it. RESULTS AND CONCLUSIONS: We found that CBX significantly reversed the EAE severity and pathology in EAE. IL-17-secreting and IFN-γ-secreting CD4+ T lymphocytes were remarkably lower in the spleen of CBX-treated mice. Production of IL-23 and IL-17 from cortex in EAE animals was markedly reduced by CBX. Furthermore, CBX treatment increased the expression of brain-derived neurotrophic factor. This study provides evidence for the protective role of CBX against EAE.
INTRODUCTION:Multiple sclerosis (MS) is a complex demyelinating disease involving central nervous system (CNS). It is still a challenge to secure an effective therapeutic strategy against this disease. Carbenoxolone (CBX) is a derivative of glycyrrhetinic acid, which is widely used in brain research for its gap-junction inhibition effects. Many researchers have observed CBX-mediated suppression of CNS inflammation in their studies. OBJECTIVE: We want to further examine its anti-inflammation effects in CNS demyelinating disease like MS. METHODS: Thus, our study applied an experimental autoimmune encephalomyelitis (EAE) mouse model and examined the effects of CBX on it. RESULTS AND CONCLUSIONS: We found that CBX significantly reversed the EAE severity and pathology in EAE. IL-17-secreting and IFN-γ-secreting CD4+ T lymphocytes were remarkably lower in the spleen of CBX-treated mice. Production of IL-23 and IL-17 from cortex in EAE animals was markedly reduced by CBX. Furthermore, CBX treatment increased the expression of brain-derived neurotrophic factor. This study provides evidence for the protective role of CBX against EAE.