Hidayat Suyuti
Laboratorium Biokimia-Biomolekuler Fakultas Kedokteran Universitas Brawijaya Malang

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HUBUNGAN ANTARA KADAR ENZIM GLUTATION REDUKTASE DENGAN DERAJAT KEKERUHAN INTI LENSA Sulistya, T Budi; Dewi, Debby Shintiya; Suyuti, Hidayat; Sumarno, Sumarno
Jurnal Kedokteran Brawijaya Vol 22, No 1 (2006)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (305.234 KB) | DOI: 10.21776/ub.jkb.2006.022.01.7

Abstract

The aim of this study was to determine the correlation between the level of glutathione reductase [GR] in relation with the severity of nuclear cataract and the increase of age. An analytic cross sectional observasional study  of nuclear cataract patient seen at Saiful Anwar Hospital and Mass Cataract Surgery performed by Perdami Malang was carried out. Patients were classified into 3 groups based on ageand 4 groups based on severity of nuclear cataract. The samples were taken by consecutive sampling and were operated on visual indication. The extracted lens were examined for [GR]. The laboratory findings of [GR] were compared with the severity of senile cataract. The data were analyzed with one way ANOVA. Confidence limit was set at 95%. A total of  55 patients were included with the sample size in 40-50 age group less than estimation. The [GR] were found to be significanfly lower in the older age (p=0,01) and the more severe cataract groups (p=0,00). The [GR] were also found to be significantly decreased with the increase of cataract severity in 40-50 age group (p=0,00), 50-60 age group (p=0,01) and >60 age group (p=0,00). In the grade 2 cataract, there were no significant difference of [GR] between age group (p=0.22). This also occured in grade 3 (p=0.23) while  in the grade 4, there were significant difference between age group (p=0.01). This also occured in grade 5 (p=0.06).
Efek Ekstrak Etanolik Daun Sirsak pada Proliferasi dan Apoptosis Sel HeLa yang Dimediasi oleh p53 Rachmawati, Ermin; Karyono, Setyawati; Suyuti, Hidayat
Jurnal Kedokteran Brawijaya Vol 27, No 1 (2012)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (620.589 KB) | DOI: 10.21776/ub.jkb.2012.027.01.5

Abstract

Kanker  serviks  merupakan  penyebab  utama  kedua  kematian  kanker  pada wanita  di seluruh  dunia, menyebabkan  240.000 kematian  setiap  tahunnya.  Ekstrak  daun  Annona  muricata  berpotensi  baik  sebagai  obat  anti  kanker .  T ujuan  dari  penelitian ini  adalah  untuk  mengetahui  pengaruh  ekstrak  etanol  daun  sirsak  (Annona  muricata)  dalam  menghambat  dan menginduksi  aktivasi apoptosis yang dimediasi oleh stabilisasi p53 pada pertumbuhan kanker serviks.  Sebuah percobaan in vitro dilakukan dengan menggunakan kultur sel HeLa. Penghambatan proliferasi diukur dengan MTT assay. Apoptosis dideteksi  dengan  menggunakan  flowcytometry  Annexin  V  Biotin  Kit  Apoptosis  Detection.  Konfirmasi  dan  perhitungan ekspresi  p53  ditentukan  oleh  imunocytochemistry.  Ekstrak  etanol  dari  daun  Annona muricata  secara  efektif  menghambat proliferasi sel HeLa dengan dosis tertentu pada paparan 48 jam. Nilai  IC50 ekstrak etanol daun Annona muricata adalah 111,75  ug/ml.  200  mg/ml  ekstrak  menginduksi  apoptosis  sel  HeLa  tergantung  dari  lama  pemaparan.  Ekstrak  ini  juga meningkatkan  ekspresi  p53  sel  HeLa  tergantung  dosis  pemberian  (25,  50,  100,  200  μg/ml)  dan  lama  pemberian  (24  dan  48 jam).  Dapat  disimpulkan  bahwa  ekstrak  etanol  daun  sirsak  menghambat  pertumbuhan  sel  HeLa  dan  menginduksi apoptosis.  Mekanisme  ekstrak  daun  sirsak  menghambat  proliferasi  dan  apoptosis  inducing  berhubungan  dengan stabilisasi  dan  aktivasi  p53.Kata  Kunci:  Daun  Annona  muricata,  apoptosis,  ekstrak  etanol,  proliferasi,  ekspresi  p53
EFEK PEMBERIAN MATRIX METALLOPROTEINASE-9 ( MMP- 9) RNA INTERFERENCE TERHADAP EKSPRESI MMP- 9 PADA KULTUR SEL ENDOTEL VASKULAR Wulandari, Lely Retno; Suyuti, Hidayat; Dewi, Nadia Artha; Refa, Safaruddin
Jurnal Kedokteran Brawijaya Vol 22, No 2 (2006)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1391.743 KB) | DOI: 10.21776/ub.jkb.2006.022.02.1

Abstract

ABSTRACT Retinal neovascularization is the main problem that causes blindness in many types of eye desease. Neovascularization occurs in ischemic retina, and several important mediators that induce neovascularization is secreted by the surrounding cell and endothelial cell vessels. Matrix metalloproteinase-9 is an enzyme secreted by endothelial cell vessels and plays an important role in the pathogenesis of retinal induce neovascularization. Vascular endothelial cells were cultured and transfected with Matrix Metalloproteinase -9 RNA interference in two doses (100nM or 200nM) and the cells were taken at 24,  48  and  72  hours.  The  expression  of  Matrix  Metalloproteinase  -9  protein  levels  were  examined  by immunocytochemistry, and compared with control group. The data were analyzed with factorial anova. Statistical analysis showed that transfection with different doses of MMP-9 RNAi gave a significant different effect on MMP-9 expression (p-value < 0.05), while exposure time did not give significant difference (p-value < 0.05). This in-vitro study indicated that transfection  of  MMP-9  RNAi  with  dose  200nM  reduced the  expression  of  MMP-9  by  50%  compared  to  the  control. Because exposure time was not significant, the lowest expression of MMP-9 can be achieved by transfecting MMP-9 RNAi 200nM for 24 hours. This is the first study that demonstrates the effectiveness of RNA interference mediated targeting  of MMP-9 to reduce the MMP-9 expression in vascular endothelial cell lines Key Words  : Matrix Metalloproteinase -9 - RNA interference - vascular endothelial cell lines.
PERAN EKSPRESI p53 DAN SURVIVIN TERHADAP HEMOGLOBIN, LEUKOSIT, DAN TROMBOSIT PADA LEUKEMIA LIMFOBLASTIK AKUT ANAK YANG MENDAPATKAN KEMOTERAPI Wairo, Candy Maharani; Nugroho, Susanto; Suyuti, Hidayat
Majalah Kesehatan FKUB Vol 6, No 1 (2019): Majalah Kesehatan
Publisher : Faculty of Medicine Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (385.737 KB) | DOI: 10.21776/ub.majalahkesehatan.006.01.3

Abstract

 Leukemia limfoblastik akut (LLA) merupakan jenis leukemia paling sering ditemukan (97%) dan menjadi penyebab kematian anak. Terapi sitostatika dapat mengakibatkan kerusakan DNA yang memicu apoptosis dengan cara menstimulasi p53 sebagai proapoptosis, menghambat survivin sebagai antiapoptosis yang berperan dalam perbaikan kadar hemoglobin, jumlah leukosit dan trombosit. Penelitian ini ingin mengungkap peran  ekspresi p53 dan survivin terhadap kadar hemoglobin, leukosit, trombosit pada LLA anak yang mendapat kemoterapi. Studi kohort prospektif dilakukan di ruang rawat inap anak RS. Dr. Saiful Anwar Malang, pada bulan April-Juni 2018. Populasi penderita LLA berdasarkan analisis morfologi darah perifer dan aspirasi bone marrow.  Deteksi  ekspresi p53 dan survivinn menggunakan metode flow cytometry. Analisis statistik menunjukkan  ekspresi p53 meningkat (p = 0,003), ekspresi survivin menurun (p = 0,000), hemoglobin (p = 0,039), leukosit (p = 0,000), trombosit (p = 0,023) meningkat. Setelah dilakukan kemoterapi, didapatkan hubungan ekspresi p53 dengan hemoglobin (p = 0,873), leukosit (p = 0,212), dan trombosit (p = 0,670) tidak signifikan. Hubungan ekspresi survivin dengan hemoglobin (p = 0,682), leukosit (p = 0,907), trombosit (p = 0,936) setelah dilakukan kemoterapi tidak signifikan. Hubungan p53 dan survivin pada pasien LLA anak sebelum kemoterapi (p = 0,005)   signifikan, namun sesudah kemoterapi (p = 0,467) tidak signifikan. Dapat disimpulkan bahwa kemoterapi meningkatkan ekspresi p53, menurunkan ekspresi survivin, dan meningkatkan kadar hemoglobin, leukosit, trombosit. Ada hubungan yang tidak signifikan antara p53 dan survivin terhadap kadar hemoglobin, leukosit, trombosit, sebelum dan sesudah kemoterapi. Didapatkan hubungan signifikan antara p53 dan survivin sebelum kemoterapi, namun tidak signifikan sesudah kemoterapi. 
Genistein Increase Intracellular Distribution of the High Motility Group Box-1 through p38 Pathway in HeLa culture cells induced by Tumor Necrosis Factor-α Herbani, Merlita; Widodo, Aris; Suyuti, Hidayat
Journal of Tropical Life Science Vol 4, No 2 (2014)
Publisher : Journal of Tropical Life Science

Show Abstract | Download Original | Original Source | Check in Google Scholar

Abstract

Cervical cancer is one kind of many cancer that cause death to women around the world. Many studies had support the statement that inflammation has a strong linkage with cancer development. Several factors like proinflammatory factor can influence tumor cell microenvironment, and induce a faster proliferation. TNF-α is suspected can induce proliferation. While cancer itself can induce inflammation, which is marked by several marker. One of them is HMGB1, released from the cell as active secretory lysosomes or passive diffusion. Genistein has demonstrated growth inhibitory effects of various types of cancer cells. It inhibits tyrosine kinase pathway, which can be activated by TNF-α. One of those pathways that have the link with proliferation is p38. This study tries to reveal about inhibitory effect of genistein toward p38 pathway that had been activated by TNF-α. This research was conducted by exposing cultured HeLa cells with various doses of genistein for 90 minutes, and then exposed to TNF - α 10 ng / mL for 20 minutes. Observations were made with a confocal microscope, by staining the cells with pp38-TRITC and HMGB1 antibody. The intensity was measured and analyzed by Fluoview software. The results suggest that there be significant differences between pp38 intranuclear intensity and HMGB1 extranuclear intensity of each dose of genistein (p = 0.000, ANOVA). pp38 and HMGB1 intensity were increased along with increasing genistein dose, but at high dose there were noted decreasing of pp38 and HMGB1 intensity. At apoptotic dose, pp38 and HMGB1 intensity were increased markedly, showing the effect of apoptosis. In general, increasing doses of genistein increase intranuclear p38 activation and HMGB1 extranuclear translocation. So there were a strong linkage between p38 activation and HMGB1 translocation in this study.