RESEARCH PAPER
Anti-epileptic drugs inhibit viability of synoviocytes in vitro
 
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1
Department of Rheumatology and Connective Tissue Diseases, Medical University, Lublin, Poland
 
2
Department of Experimental and Clinical Pharmacology, Medical University, Lublin, Poland
 
3
Department of Orthopedics and Rehabilitation, Medical University, Lublin, Poland
 
4
Department of Toxicology, Institute of Rural Health, Lublin, Poland
 
5
Department of Medical Biology, Institute of Rural Health, Lublin, Poland
 
6
Department of Virology and Immunology, Institute of Microbiology and Biotechnology, Maria Curie-Sklodowska University, Lublin, Poland
 
 
Corresponding author
Jolanta Parada-Turska   

Department of Rheumatology and Connective Tissue Diseases, Medical University, Lublin, Poland
 
 
Ann Agric Environ Med. 2013;20(3):571-574
 
KEYWORDS
ABSTRACT
Introduction:
The hyperplasia of synovial fibroblasts is considered to be essential for the evolution of joint destruction in rheumatoid arthritis (RA). Previously, we reported that anti-rheumatic drugs, both COX inhibitors and disease-modifying anti-rheumatic drugs inhibit proliferation of synoviocytes in vitro. The presented study investigates the effect of anti-epileptic drugs on the viability and proliferation of synovial fibroblasts in vitro.

Material and Methods:
Experiments were conducted on human synoviocytes derived from an RA patient and rabbit synoviocytes cell line HIG-82. Cell proliferation and viability were assessed by means of BrdU assay and MTT assay, respectively. The IC50 value (the concentration of drug necessary to induce 50% inhibition) together with confidence limits was calculated.

Results:
Carbamazepine inhibited proliferation of human fibroblasts and viability of HIG-82 with IC50 values of 86 µM and 82 µM, respectively. Diphenylhydantoin, valproate and phenobarbital inhibited viability of HIG-82 cells with the IC50 values of 110, 500 and 1031 µM, respectively.

Conclusions:
Based on these findings, it can be suggested that anti-epileptic drugs may have a disease-modifying effect on rheumatoid synovial proliferation.

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