Latar belakang: Gangguan induksi penuaan saat penyembuhan luka dapat menimbulkan keloid. Bahan yang memacu penuaan fibroblas dapat digunakan untuk mencegah keloid. Triamsinolon asetonida (TA) atau mitomisin C (MMC) dapat memperbaiki keloid melalui pengurangan proliferasi fibroblas yang juga merupakan ciri penuaan selular.
      Tujuan: Mengetahui efek TA atau MMC terhadap peningkatan ekspresi penanda penuaan SA-αgal fibroblas keloid, dosis optimal TA atau MMC serta perbedaan potensi antara TA dan MMC dalam memacu peningkatan ekspresi SA-βgal.
        Metode: Biakan fibroblas keloid subkultur ke-3 dibagi menjadi 8 kelompok perlakuan: plasebo, 150 μM H2O2 (kontrol prosedur), TA dosis 10, 20, 40 μM, dan MMC dosis 0,015; 0,03; 0,06 μM. Pada setiap kelompok dilakukan pewarnaan SA-βgal. Perbandingan rerata persentase sel positif SA-βgal terhadap populasi total masing-masing kelompok dianalisis dengan uji ANOVA satu arah.
       Hasil: H2O2 dosis 150 μM meningkatkan ekspresi penanda penuaan SA-βgal fibroblas keloid secara bermakna (p<0,05), menunjukkan prosedur berlangsung benar. Triamsinolon asetonida 10, 20, dan 40 μM meningkatkan ekspresi SA-βgal secara bermakna (p<0,05) dengan dosis optimal 20 μM. Hanya MMC dosis 0,015 μM yang meningkatkan ekspresi SA-βgal secara bermakna (p<0,05). Mitomisin C dosis 0,015 μM mengekspresikan SA-βgal lebih tinggi secara bermakna dibandingkan dengan 20 μM TA (p<0,05).
       Simpulan: TA atau MMC meningkatkan ekspresi penanda penuaan SA-αgal fibroblas keloid bergantung pada dosis. Dosis optimal TA dan MMC masing-masing adalah 20 μM dan 0,015 μM. Mitomisin C lebih kuat memacu peningkatan ekspresi penanda penuaan SA-βgal fibroblas keloid daripada TA. (MDVI 2011; 38/s; 24s - 29s)

Kata kunci : keloid, penuaan, SA-βgal, triamsinolon asetonida, mitomisin C, fibroblas

       Background: The defective induction of senescence may provoke keloid. Therapy that induces fibroblasts senescence can be used to prevent the keloid. Triamcinolon acetonide (TA) or mitomycin C (MMC) can improve keloid by decreasing fibroblasts proliferation that is also the characteristic of cellular senescence.
       Objective: To know the effect of TA or MMC on the increased of the SA-αgal senescencemarker expression of keloid fibroblasts, the optimum dose of TA or MMC and the potential difference in increasing the SA-βgal expression between the use of TA and MMC.
       Method: Passage III keloid fibroblasts culture was divided into 8 groups of treatment: placebo, 150 μM H2O2, TA (10, 20, 40 μM), and MMC (0,015; 0,03; 0,06 μM). Each group was stained by SA-βgal. The average ratio of positive cells towards total population of each groups was analysed by one-way ANOVA.
       Result: 150 μM H2O2 increased the SA-βgal senescence-marker expression of keloid fibroblasts
significantly (p<0,05), it showed that the procedure was correct. The use of 10, 20, 40 uM TA increased the SA-βgal expression of keloid fibroblasts significantly (p<0,05) with the optimum dose 20 μM. Moreover, only 0,015 μM mitomysin C which showed increased of the expression significantly (p< 0,05). The application of 0,015 μM MMC had a stronger effect to increase the expression of SA-βgal than 20 uM TA significantly (p<0,05).
      Conclusion: TA or MMC increased the SA-αgal senescence-marker expression of keloid fibroblasts depending on dose. The optimum dose of TA and MMC were 20 μM and 0,015 μM, respectively. Mitomysin C provided a stronger effect on the increased of the SA-βgal senescencemarker expression of fibroblasts keloid compared to TA.(MDVI 2011; 38/s; 24s - 29s)

Keywords: keloid, senescence, SA-βgal, triamcinolone acetonide, mitomycin C, fibroblast