Articles
<![CDATA[α-Lipoic acid inhibit the decrease of collagen deposition in ultravioled B-irradiated cultured normal human skin fibroblasts cell culture ]]>
<![CDATA[Arum Krismi Satiti Retno Pudjiati Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 43, No 02 (2011) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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<![CDATA[Repeated ultraviolet B (UVB) irradiation on human skin has been considered to be responsible in premature agingprocess because UVB has been proved to inhibit collagen deposition and accelerates collagen degradation. Clinicalstudies showed that topical usage of 5% α-lipoic acid (ALA) improved the clinical appearance of photoaged skin.However, the effect of ALA on collagen deposition and degradation in UVB-irradiated normal human skin fibroblastsculture has not been reported. The aim of the study was to investigate the effect of ALA on collagen deposition anddegradation in UVB-irradiated cultured normal human skin fibroblasts. Culture of normal human skin fibroblasts weretreated with 0, 125, 250, 500 μM ALA diluted in complete Dulbecco’s Modified Eagle’s Medium (DMEM) andirradiated with 300 mJ/cm2 UVB. The mean collagen deposition and degradation’s level were measured by Siriusred assay and read with spectrophotometer at λ 550 nm. Mean difference of collagen deposition as expressed byoptical density (OD) between normal human skin fibroblasts cell after UVB irradiation and without UVB irradiationwas analyzed by Wilcoxon signed-ranks test and Friedman test, while mean difference collagen degradation wasanalyzed by one way analysis of variance (ANOVA) and paired t test with 95% confidence level (p<0.05). Theresults showed that ALA 125 μM inhibited the decrease of collagen deposition significantly (p<0.05), though higherconcentrations did not. However, ALA did not inhibit collagen degradation increment (p>0.05). In conclusion, ALAinhibited the decrease of collagen deposition, but did not inhibit collagen degradation in UVB-irradiated normalhuman skin fibroblasts culture.Key words: α-lipoic acid - collagen - human skin - fibroblasts – UVB - irradiation]]>
<![CDATA[The effect povidone-iodine on the wound healing process: A study on fibroblast populated collagen lattice (FPCL) model ]]>
<![CDATA[Retno Danarti]]>;
<![CDATA[. Suswardana]]>;
<![CDATA[Arief Budiyanto]]>;
<![CDATA[Widodo Wirohadidjojo]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 46, No 03 (2014) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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DOI: 10.19106/JMedScie.004603201401
<![CDATA[Povidone-iodine (PI) 10% solution is an effective antiseptic. However, it appears to be toxic tothe cells involved in wound healing. The aim of this study is to evaluate the toxicity of PI oncultured human fibroblast using fibroblast populated collagen lattice (FPCL) model. The culturedhuman fibroblast was divided into 6 groups i.e. 5 groups were exposed by PI 1, 0.1, 0.01, 0.001and 0.0001%, and 1 group was exposed by phosphate-buffered-saline (PBS). Twenty-four hourslater, the media was washed using PBS. The size of the FPCL media on each group wasobserved over time by serial photographs, which then were measured by Image-J computerprogram. Exposure of 0.1, 0.01, 0.001 and 0.0001 PI caused an obvious reduction of fibroblast’scontraction capability on FPCL media, which described temporary fibroblast injury, that showinga concentration-dependent recovery phenomenon after 48th hour. Furthermore, 1% PI exposureleads to a permanent fibroblast injury. In conclusion, PI exposure in concentration more than0.1% has a permanent toxic effect on fibroblast that clearly observed using a simple FPCLmodel.]]>
<![CDATA[Transplantation of melanocyte stem cells in vitiliginous skin ]]>
<![CDATA[Yohanes Widodo Wirohadidjojo]]>;
<![CDATA[Flandiana Yogianti]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 47, No 4 (2015) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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DOI: 10.19106/JMedSci004704201503
<![CDATA[Depigmentation in vitiligo occurs as a result of progressive loss of functioning epidermal melanocytes, and currently various modalities have been developed to re-functioning these cells. However, in area with poor melanocytes reservoir, such as old-persistent lesions or lesions on bony prominence, the modalities are hardly to achieve repigmentation. Since spontaneous repigmentation of vitiliginous skins begin mostly in follicular areas, reactivation of melanocyte precursors along the outer root sheath of hair follicle is expected to have better on this pigmentation. Melanocyte precursor came from melanocyte stem cells that originally located on bulge area of hair follicles. The latest surgical intervention in vitiligo is transplantation of melanocyte stem cells. Clinical experiments indicated that the transplantation can be performed either by transplantation of extracted follicular units or single cell suspension harvested from this area. By single cell suspension treatment, a 50 cm2 of vitiliginous skin can be handled by 15 autologous hair follicular units. These procedures are easy and can be performed by any dermatologist especially who has been trained in dermatologic surgery as well as in cellular based therapies.]]>
<![CDATA[The Effect of PRF on Serum Starved Human Dermal Fibroblast. ]]>
<![CDATA[Sunardi Radiono]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>;
<![CDATA[Arief Budiyanto]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 2 (2016) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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DOI: 10.19106/JMedSci004802201605
<![CDATA[ABSTRACTHealing failure on chronic ulcers was suspected due to the decrease of Growth Factors (GFs) supply caused by either GFs trapped in the fibrin, or degraded by protease, or decreased level due to reduction of GFs gene expression. Administration of various GFs can stimulate healing of chronic ulcers. High level of GFs is available in biologic material called Platelet Rich Fibrin (PRF). This study was conducted to have in vitro evidence of PRF effect on GFs-serum starved human dermal fibroblasts as representative cells of chronic ulcers. Human dermal fibroblasts (HDFs) were isolated from foreskin of six boys aged 11- 14 years-old. After 24 hours of serum deprivation, HDFs were treated by 100, 50, and 25% PRF lysate diluted in cultured medium. Cellular migration was measured using scratch assay, while cellular viability was measured using MTT assay and collagen deposition was measured using Sirius Red assay. The HDFs of serum starvation group showed significant impairment activities in terms of cellular migration (25%), cellular proliferation (20%), and collagen deposition (10%) (p<0.05). Administration with various levels of PRF lysate could significantly recover those activities (p < 0.05). Because cellular activities of serum starved HDFs is similar with fibroblasts isolated from the bottom of chronic ulcers and administration of various levels of PRF lysate was capable to recover those activities, it can be concluded that PRF is a good biologic material to stimulate healing of chronic ulcers. However, in order to get better evidence based medicine, both pre clinical and clinical studies must be performed.]]>
<![CDATA[The effect of mitomycin-c in keloid fibroblast cultures ]]>
<![CDATA[Ishandono Dachlan]]>;
<![CDATA[Teguh Aryandono]]>;
<![CDATA[Mae Sri Hartati Wahyuningsih]]>;
<![CDATA[Hardyanto Soebono]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 3 (2016) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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DOI: 10.19106/JMedSci004803201605
<![CDATA[ABSTRACTKeloid occurs due to hyperactivity of keloid fibroblast (KF) in proliferation, migration, collagen deposition, together with low rates of collagen degradation. These are under the responsibility of TGF-b. Mitomycin C (MC) is used for treating keloid by a topical application during surgery at the level of 0.02% to 0.08%. Unfortunately, the lowest effective level of MC for keloid has not been determined yet. We aimed to determine the lowest effective level of MC in the suppression of KF activities. Various levels of MC diluted in growth medium were administered on KF that were isolated from six patients. After 24 hours and 72 hours of incubation, cellular proliferation, collagen deposition, cellular migration and level of TGF-b, were analyzed. Application of 120 uM MC on KF culture for 24 hours could significantly reduce TGF-b production from 1265.74 ± 274.81 pg/mL to 265.17 ± 12.20 pg/mL; proliferation index from 100% to 84.01 ± 12.91%; inhibit cellular migration to 64.38 ± 3.66%; but reduce collagen depositions from 100% to only 91.13 ± 10.19%. The lowest MC level is on 30 uM or equal with 0.001%. In conclusion, the lowest level of MC can suppress the activities of KF is 0.001%. Moreover, due to low activity in inhibiting collagen deposition, MC would be better as an adjuvant drug for keloid surgery.]]>
<![CDATA[The effect of combination of triamcinolone acetonide and methotrexate on keloidfibroblast activity in dermis equivalent ]]>
<![CDATA[Endra Yustin E. S]]>;
<![CDATA[Fajar Waskito]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 40, No 02 (2008) ]]>
Publisher : <![CDATA[Journal of the Medical Sciences (Berkala Ilmu Kedokteran) ]]>
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<![CDATA[Background: Triamcinolone acetonid (TA) intralesion has been a standard treatment for keloids for manyyears, due to its effect in inhibiting collagen synthesis and fibroblast proliferation. However, until now theclinical result is unsatisfactory. Keloid flattening is slow and sometimes adverse reactions may occur.Methotrexate (MTX) is a chemotherapeutic agent having an antiproliferating effect which act as an antifolicacid. Because of this effect, MTX is potential to be used in combination with TA for the treatment inkeloid. Fibroblast populated collagen lattice (FPCL) was a dermal equivalent usually used for fibroblastactivity measurement.Objective: To understand the inhibition of fibroblast keloid activities of MTX in vitro on FPCL contraction,compared to TA and MTX plus TA.Methods: This research used simple parallel multigroups experimental study design, and conducted on thirdpassage keloid fibroblast culture, which was isolated from one patient. Fibroblast was cultivated in collagentype 1 from rat tail (FPCL). Keloid fibroblasts was classified into 16 groups, and treated with 5, 10, 20mM TA, 1.75, 3.5, 7 mM MTX, combination of TA and MTX, and a control negative. FPCL contractionindicating activities of fibroblast was measured using Scion Image software. Mean of FPCL contractionwas analyzed using one way analysis of variance (ANOVA).Results: All treatments could inhibit FPCL contraction until day 2 (p<0.05). The highest inhibition of FPCLwas found in combination of TA 20 mM + MTX 7 mM (p<0.05). The treatment that could inhibit FPCLcontraction until day 3 was only group MTX 3.5 mM + TA 20 mM. This result indicated that a combinationof TA and MTX was stronger in inhibiting keloid fibroblast activities compared with TA and MTX alone.Key words: keloid fibroblast - growth factors - triamcinolone acetonid - methotrexate - FPCL contraction]]>
<![CDATA[Pseudolimfoma Kutis: Laporan Kasus ]]>
<![CDATA[Kartika Kemala]]>;
<![CDATA[Wening Setyani]]>;
<![CDATA[Dyah Ayu Mira Oktarina]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ Berkala Ilmu Kesehatan Kulit dan Kelamin Vol. 30 No. 3 (2018): DESEMBER ]]>
Publisher : <![CDATA[Faculty of Medicine, Universitas Airlangga ]]>
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DOI: 10.20473/bikk.V30.3.2018.275-278
<![CDATA[Latar Belakang: Pseudolimfoma kutis adalah proses limfoproliferatif jinak poliklonal pada kulit, yang menyerupai limfoma kutis secara klinis dan atau histopatologi. Pseudolimfoma kutis bermanifestasi dalam bentuk nodul atau plak keunguan pada wajah. Pada kasus yang dicurigai sebagai pseudolimfoma kutis, bagian terpenting adalah diagnosis untuk membedakan lesi tersebut jinak atau ganas. Diagnosis memerlukan kombinasi antara pemeriksaan klinis, histopatologis, dan imunohistokimia. Tujuan: Melaporkan satu kasus pseudolimfoma kutis yang menitikberatkan pada masalah penegakan diagnosis. Kasus: Seorang wanita usia 27 tahun, datang dengan keluhan nodul asimptomatik berwarna merah pada pipi sejak 2 bulan yang lalu. Pemeriksaan histopatologi didapatkan sebukan limfosit padat membentuk folikel limfoid dengan centrum germinativum yang sebagian mendestruksi kelenjar appendices kulit dan meluas hingga jaringan lemak subkutis. Pemeriksaan imunohistokimia menunjukkan hasil positif dengan pewarnaan cluster of differentiation (CD) 20+, CD3+, dengan dominasi pada CD3+. Pewarnaan CD4+ menunjukkan hasil positif dan CD8+ dengan hasil negatif. Penatalaksanaan: Pasien diterapi dengan injeksi triamsinolon asetonid 10 mg/ml intralesi, dan memberikan hasil yang memuaskan setelah 3 kali injeksi. Simpulan: Berdasarkan anamnesis, pemeriksaan fisik, pemeriksaan histopatologi, dan imunohistokimia, telah ditegakkan kasus pseudolimfoma kutis pada seorang wanita 27 tahun. Terapi dengan injeksi triamsinolon asetonid 10 mg/ml intralesi memberikan hasil yang memuaskan.]]>
<![CDATA[Peran Sinar Matahari terhadap Derajat Keparahan dan Progresivitas Penyakit Vitiligo ]]>
<![CDATA[Tuntas Rayinda]]>;
<![CDATA[Prasta Bayu Putra]]>;
<![CDATA[Sunardi Radiono]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ Berkala Ilmu Kesehatan Kulit dan Kelamin Vol. 31 No. 3 (2019): DESEMBER ]]>
Publisher : <![CDATA[Faculty of Medicine, Universitas Airlangga ]]>
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DOI: 10.20473/bikk.V31.3.2019.116-121
<![CDATA[Latar belakang: Peran sinar matahari dalam vitiligo belum sepenuhnya dipahami. Terapi ultraviolet merupakan salah satu terapi yang efektif untuk vitiligo. Akan tetapi, teori lain mengatakan bahwa peningkatan reactive oxygen species (ROS) yang diinduksi oleh paparan sinar matahari dapat menyebabkan kerusakan tirosinase dan sensitisasi sel T. Simple 1-week sun exposure recall (S1WSER) merupakan kuesioner yang telah digunakan untuk memprediksi sirkulasi 25-hidroksivitamin D pada ras Kaukasia dengan menghitung jumlah paparan sinar matahari harian. Tujuan: Mengevaluasi peran sinar matahari pada derajat keparahan dan progresivitas penyakit vitiligo. Metode: Sebanyak 22 pasien vitiligo yang menjalani narrow band ultraviolet-B (NBUVB) seluruh tubuh diminta untuk menilai jumlah paparan sinar matahari harian menggunakan S1WSER. Progresivitas penyakit didapatkan dari perbedaan antara nilai Self Assessed Vitiligo Area Severity Index (SAVASI) berdasar kondisi kulit sebelum memulai fototerapi dan kondisi lesi kulit saat ini (ΔSAVASI). Keparahan penyakit didapatkan dari skor Vitiligo Area Scoring Index (VASI) yang dinilai oleh dokter. Hasil: Jumlah area tubuh yang terpapar oleh sinar matahari atau Total Body Areas Exposed by Sunlight (TBAES) dan total skor S1WSER lebih tinggi pada kelompok pasien vitiligo, yang menunjukkan perbaikan setelah foterapi NBUVB dibandingkan kelompok yang tidak mengalami perbaikan (p<0.05). Korelasi negatif ditemukan antara TBAES dan ΔSAVASI (p<0,05, r=-0,457), meskipun demikian total skor S1WSER dan jumlah waktu terpapar sinar matahari Total Time Exposed by Sunlight (TTES) tidak berkorelasi dengan ΔSAVASI (p>0.05). Tidak didapatkan korelasi yang signifikan antara skor VASI dan skor total S1WSER, TBAES, atau TTES (p>0.05). Simpulan: Sinar matahari memperlambat progresifitas penyakit vitiligo. Derajat keparahan vitiligo tidak berkorelasi dengan jumlah dan waktu paparan sinar matahari.]]>
<![CDATA[The cytotoxic effect of pinostrobin fingerroot (boesenbergia pandurata)on the culture of hela cells ]]>
<![CDATA[Rosmelia Rosmelia]]>;
<![CDATA[Betty Ekawati Suryaningsih]]>;
<![CDATA[Hady Anshory]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>
<![CDATA[ JKKI : Jurnal Kedokteran dan Kesehatan Indonesia JKKI, Vol 7, No 4, (2016) ]]>
Publisher : <![CDATA[Faculty of Medicine, Universitas Islam Indonesia ]]>
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DOI: 10.20885/JKKI.Vol7.Iss4.art4
<![CDATA[Background : Cancer is one of the leading causes of death worldwide, therefore struggles to find more effective treatment and prevention is needed. Several studies has been performed using natural ingredients, one of which is Temu Kunci (B. pandurata). Temu Kunci extract contains flavonoid pinostrobin that has been showed as having cytotoxicity effects. Cytotoxicity tests of pinostrobin have been performed on several tumor cell lines, but its cytotoxicity effect on HeLa cell line has never been reported. Objective : To assess cytotoxicity effect of pinostrobin temu kunci on HeLa cell culture Methods : This study used simple experimental design. Pinostrobin were isolated from temu kunci and proved by TLC densitometry compared to standard pinostrobin. HeLa cell culture were treated with pinostrobin with concentrations 5, 25, 50, 75, 100, and 250 ug/mL. Cytotoxicity test were performed by MTT assay. Data were analyzed using one-way ANOVA. Results : There was significant difference (p=0.000) of means of cell viability percentage, respectively: 92.58 ± 9.84 (5μg/mL), 91.78 ± 4.4 (25μg/mL), 80.09 ± 4.51 (50μg/mL), 76.89 ± 7.75 (75μg/mL), 67.85 ± 11.31 (100μg/mL), dan 48.82 ± 16.61 (250μg/mL). The IC50 was 250μg/mL. Conclusion : Pinostrobin showed no active cytotoxicity effect on HeLa cell culture.]]>
<![CDATA[The efficacy of captopril and 5-fluorouracil combination in the proliferation and collagen deposition of keloid fibroblast ]]>
<![CDATA[Jesslyn Amelia]]>;
<![CDATA[Yohanes Widodo Wirohadidjojo]]>;
<![CDATA[Agnes Sri Siswati]]>
<![CDATA[ Indonesian Journal of Biotechnology Vol 27, No 3 (2022) ]]>
Publisher : <![CDATA[Universitas Gadjah Mada ]]>
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DOI: 10.22146/ijbiotech.69505
<![CDATA[Keloid is a benign fibroproliferative tissue growth that exceeds the initial wound margins. Captopril has been tested in vitro to reduce fibroblast proliferation and collagen deposition; thus, it has potential for use in the treatment of keloids. Meanwhile, 5‐fluorouracil (5‐FU) has already been used in keloid management. This study aimed to determine the efficacy of the combination of captopril and 5‐FU in keloid fibroblast cultures. Keloid tissues were cultured up to passages 4–7. The study consisted of a control group, captopril in various concentrations (10‐2, 10‐3, 10‐4, and 10‐5 mol/L), 5‐FU 1 mg/mL and a combination of captopril at various concentrations with 5‐FU 1 mg/mL. After 144 hours of treatment, fibroblast proliferation and collagen deposition were measured. The study showed a significant decrease in the mean index of fibroblast proliferation and collagen deposition in the group receiving captopril in various concentrations (10‐2, 10‐3, 10‐4, and 10‐5 mol/L) and the 5‐FU group against the control group (p<0.05). In the combined‐dose group, captopril at a concentration of 10‐2 mol/L and 5‐FU showed a significant reduction in fibroblast proliferation and collagen deposition compared to the 5‐FU group and the captopril at the same dose (p<0.05). In conclusion, the combination of captopril 10‐2 mol/L and 5‐FU 1 mg/mL is better at reducing fibroblast proliferation and collagen deposition in keloid fibroblast cultures than captopril or 5‐FU as a single therapeutic agent.]]>
