Abstract
Extensive scarring normally causes hypertrophic or keloid scars. This intuitively results in psychosocial distress and reduction in life quality. Tripterine is a bioactive pentacyclic triterpenoid compound while it is still poorly understood whether it possesses an anti-scarring function. NIH/3T3 cells were administrated with tripterine at increased concentrations (0-10 μM). Antisense RNA to INK4 locus (ANRIL) was transformed into NIH/3T3 cells, and the cells transfected with empty vector (mock transfection) were used as negative control. Then, cell viability and migration were profiled by cell counting kit-8 (CCK-8) and 24-Transwell assay. Protein expression was analyzed by Western blot assay. ANRIL was quantified by quantitative reverse transcription-PCR (qRT-PCR). Tripterine administration induced the growth inhibition of NIH/3T3 cells indicated by a trend toward the decreased expression of matrix metallopeptidase (MMPs), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). This process was accompanied by the decreased phosphorylation of p65, inhibitor of nuclear factor kappa-B alpha (IκBα) and the downregulation of β-catenin. Moreover, ANRIL expression was notably repressed by tripterine. By contrast, in ANRIL-transfected cells, the effect of tripterine was abolished. Tripterine exhibited an anti-scarring bioactivity in NIH/3T3 cells by inhibiting ANRIL, and this process was accompanied by the blockade of nuclear factor-kappa B (NF-κB) and β-catenin cascades.