The Anti-Inflammatory Effects of Oral-Formulated Tacrolimus in Mice with Experimental Autoimmune Encephalomyelitis.
Myung Jin KimJung Joon SungSeung Hyun KimJeong Min KimJung-Joon SungSeog Kyun MunSuk Won AhnPublished in: Journal of Korean medical science (2018)
Multiple sclerosis (MS) is a T-lymphocyte-mediated autoimmune disease that is characterized by inflammation in the central nervous system (CNS). Although many disease-modifying therapies (DMTs) are presumed effective in patients with MS, studies on the efficacy and safety of DMTs for preventing MS relapse are limited. Therefore, we tested the immunosuppressive anti-inflammatory effects of oral-formulated tacrolimus (FK506) on MS in a mouse model of experimental autoimmune encephalomyelitis (EAE). The mice were randomly divided into 3 experimental groups: an untreated EAE group, a low-dose tacrolimus-treated EAE group, and a high-dose tacrolimus-treated EAE group. After autoimmunization of the EAE mice with myelin oligodendrocyte glycoprotein, symptom severity scores, immunohistochemistry of the myelination of the spinal cord, and western blotting were used to evaluate the EAE mice. After the autoimmunization, the symptom scores of each EAE group significantly differed at times. The group treated with the larger tacrolimus dose had the lowest symptom scores. The tacrolimus-treated EAE groups exhibited less demyelination and inflammation and weak immunoreactivity for all of the immunization biomarkers. Our results revealed that oral-formulated tacrolimus inhibited the autoimmunization in MS pathogenesis by inactivating inflammatory cells.
Keyphrases
- multiple sclerosis
- mass spectrometry
- low dose
- ms ms
- high dose
- high fat diet induced
- spinal cord
- oxidative stress
- mouse model
- white matter
- induced apoptosis
- type diabetes
- spinal cord injury
- blood brain barrier
- metabolic syndrome
- adipose tissue
- skeletal muscle
- neuropathic pain
- insulin resistance
- newly diagnosed
- stem cell transplantation
- cell cycle arrest
- cell death
- cell proliferation
- signaling pathway