BASIC RESEARCH
Evaluation of the effects of pregabalin on chondrocyte proliferation and CHAD, HIF-1α, and COL2A1 gene expression
 
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Submission date: 2017-11-25
 
 
Final revision date: 2018-01-02
 
 
Acceptance date: 2018-01-03
 
 
Online publication date: 2018-02-02
 
 
Publication date: 2018-10-31
 
 
Arch Med Sci 2018;14(6):1340-1347
 
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ABSTRACT
Introduction:
The aim of the present study is to investigate the effects of pregabalin (PGB) on chondrocyte proliferation and collagen type II (COL2A1), hypoxia-inducible factor 1- (HIF-1), and chondroadherin (CHAD) gene expression in osteoarthritic chondrocytes.

Material and methods:
Standard primary chondrocyte cultures were prepared using osteochondral tissues that were surgically obtained from 6 patients with gonarthrosis. Cell morphology was evaluated using an inverted microscope, and cell death and proliferation were determined through MTT analysis, which was confirmed by AO/PI staining and statistically evaluated. The expression levels of CHAD, COL2A1, and HIF-1 genes were assessed using gene-specific TaqMan Gene Expression Assays.

Results:
MTT analyses showed that PGB administration did not have a negative or toxic effect on cell viability and proliferation in cultured chondrocytes (p < 0.001), but in our morphological evaluation extracellular matrix development was observed to be weaker in cultures treated with PGB. After 24 h of treatment, COL2A1, HIF-1, and CHAD gene expression decreased in the groups to which PGB was applied compared to gene expression before the experiment (at 0 h); at 48 h, CHAD and HIF-1 expression increased to the same level as the control group, but the expression of COL2A1 continued to decrease.

Conclusions:
Further studies need to be conducted with more participants to prove that there is a negative correlation between extracellular matrix formation and PGB administration. Our preliminary data show that even at low doses and over short-term administration, PGB may affect chondrocyte cells at the gene-expression level.

eISSN:1896-9151
ISSN:1734-1922
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