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All Journal Jurnal Ilmu Kedokteran (Journal of Medical Science) Health Science Journal of Indonesia Jurnal Keperawatan Respati Yogyakarta Indonesian Journal of Biomedicine and Clinical Sciences

Nur Arfian

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Author-ID : 2741510

Biochemistry, Genetics & Molecular Biology Dentistry Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience Nursing Public Health

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Articles

Ethanol Extracts of Centella asiatica (L.) Urb. Leaf Increase Superoxide Dismutase-2 (SOD-2) Expression on Rat Cerebellar Purkinje Cells After Chronic Stress Desby Juananda; Dwi Cahyani Ratna Sari; Mawaddah Ar-Rochmah; Nur Arfian; Muhammad Mansyur Romi
Jurnal Ilmu Kedokteran Vol 11, No 2 (2017): Jurnal Ilmu Kedokteran
Publisher : Fakultas Kedokteran Universitas Riau

Beberapa penelitian menunjukkan bahwa stres kronis meningkatkan produksi reactive oxygen species (ROS), dan /atau menekan mekanisme pertahanan antioksidan. Efek neuroprotektif dari Centella asiatica (L.). Urb telah dilaporkandapat melindungi neuron dari kerusakan oksidatif. Tujuan dari penelitian ini adalah untuk mengetahui efek ekstraketanol C. asiatica leaf terhadap ekspresi superoxide dismutase-2 sel (SOD- 2) pada sel Purkinje serebelum tikussetelah diberikan kejutan kronis di kaki. Sebanyak 25 tikus Sprague Dawley jantan dewasa muda diacak ke dalam limakelompok. Kelompok kontrol negatif terdiri dari tikus yang tidak stres; kelompok kontrol stres menerima aquadest; dankelompok lain diobati dengan dosis yang berbeda (mg / kg berat badan / hari, p.o.) ekstrak etanol daun C. asiatica: 150,300 dan 600, masing-masing diikuti oleh pemberian kejutan kronis di kaki selama dua puluh delapan hari. Ekspresi SOD-2 dari lapisan sel Purkinje diukur menggunakan metode imunohistokimia. Data dianalisis dengan one-way ANOVA (p<0,05). Kami menemukan bahwa ekspresi SOD-2 (%) dari lapisan sel Purkinje untuk kelompok kontrol negatif, kelompokkontrol stres, CeA150, CeA300 dan CeA600 kelompok adalah 22,38 ± 9,73, 9,81 ± 2,21, 10,29 ± 3,60, 14,72 ± 6,65, dan22,75 ± 10,93, masing-masing (p <0,05). Analisis post-hoc menunjukkan perbedaan yang signifikan antara kelompokkontrol negatif dan kelompok kontrol stres (p <0,05). Ada juga perbedaan yang signifikan antara kelompok kontrolstres dan kelompok CeA600 (p <0,05), tetapi tidak ada perbedaan yang signifikan antara kelompok perlakuan (p> 0,05).Penelitian ini menunjukkan bahwa ekstrak etanol daun C. asiatica meningkatkan ekspresi SOD-2 pada sel Purkinjecerebellar tikus setelah stres kronis.

Pengaruh Stres Kronik terhadap Otak: Kajian Biomolekuler Hormon Glukokortikoid dan Regulasi Brain-Derived Neurotrophic Factor (BDNF) Pascastres di Cerebellum Desby Juananda; Dwi Cahyani Ratna Sari; Djoko Prakosa2,; Nur Arfian; Mansyur Romi
Jurnal Ilmu Kedokteran Vol 9, No 2 (2015): Jurnal Ilmu Kedokteran
Publisher : Fakultas Kedokteran Universitas Riau

The brain is the central organ of stress adaptation, and is also a target of stress. Chronic stress may result in abnormalchanges in brain plasticity; include dendritic retraction, neuronal toxicity, and suppression of neurogenesis andaxospinous synaptic plasticity. Repetitive stress exposure will gradually change the electrical characteristic, morphologyand proliferative capacity of neurons. Among brain region, the cerebellum is known to be severely affected by oxidativedamage associated with glucocorticoids level. It is believed due to the highest levels of glucocorticoid receptorslocalized in the external granular layer. BDNF, a member of neurotrophin family, is known to be a strong survivalpromoting factor, and plays a critical role in cell proliferation and differentiation, neuronal protection, and the regulationof synaptic function in the central nervous system. BDNF is highly expressed in the cerebellum, mainly in granulecells. Both acute and chronic stress change BDNF expression in the brain. Although the impact of stress on BDNFlevels showed the different results, BDNF is believed to protect neurons from injuries caused by stress.

Overexpression of MiR-155-5p and increased number of macrophage population in precancerous prostatic disease Rachma Greta Putri; Sari Eka Pratiwi; Didik Setyo Heriyanto; Danarto Danarto; Indwiani Astuti; Nur Arfian; Sofia Mubarika Haryana
Health Science Journal of Indonesia Vol 11 No 2 (2020)
Publisher : Sekretariat Badan Penelitian dan Pengembangan Kesehatan

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22435/hsji.v11i2.3952

Latar Belakang: Gangguan regulasi mikroRNA(miR) dan inflamasi kronik dapat mengubah tumor menjadi karsinoma dan kanker dengan metastasis melalui perubahan seluler dan genomik. Lesi prekanker memiliki peluang 33,3 persen menjadi kanker. Penelitian ini bertujuan untuk mengkaji peran miR-155-5p terhadap mRNA SOCS1 dan populasi makrofag terhadap progresivitas penyakit yang berhubungan dengan Benign Prostate Hyperplasia (BPH), High Grade Prostatic Intraepithelial Neoplasia (HGPIN), dan Prostate Adenocarcinoma (PRAD). Metode: Penelitian ini merupakan penelitian potong lintang dengan 3 kelompok, yaitu BPH,HGPIN, dan PRAD. Sampel jaringan didapatkan dari Tindakan TURP. Ekspresi miR-155 dianalisis menggunakan qPCR dan dikalkulasi menggunakan metode Livak. Ekspresi mRNA SOCS-1 dianalisis menggunakan reverse transcriptase PCR. Penanda pan makrofag, anti CD-68 monoclonal antibody(MoAb) digunakan untuk mendeteksi populasi makrofag pada jaringan dengan imunohistokimia. Hasil: Ekspresi miR-155 lebih tinggi pada HGPIN dibandingkan BPH dan PRAD (p=0,14). Ekspresi mRNA SOCS1 pada HGPIN paling rendah diantara ketiga sampel (p=0,96). Terdapat korelasi negative antara miR-155 dan mRNA SOCS1 (p=0,02). Terdapat peningkatan persentase populasi makrofag yang signifikan pada HGPIN (6,03 persen) dibandingkan BPH (0.89 persen) dengan p=0,00. Kesimpulan: Pada penelitian ini, terdapat perubahan persentase makrofag dan miR-155 pada HGPIN. Variasi ekspresi miR-155 dan persentase populasi makrofag dapat disebabkan karena perubahan epigenetik. Oleh sebab itu, perlu penelitian lebih lanjut untuk memvalidasi hasil tersebut dan memahami kemungkinan menjadi biomarker pada penyakit prekanker pada prostat. Kata Kunci: Prostatic Intaepithelial Neoplasia, miR-155, Makrofag Abstract Background: Impaired microRNA(miR) regulation and chronic inflammation could transform tumors into carcinoma and cancer by metastasis through cellular and genomic changes. Precancerous lesions have a 33.3 percent chance of becoming cancerous. This study investigated the role of miR-155 related to SOCS1 mRNA and macrophage population in disease progression associated with Benign Prostate Hyperplasia (BPH), High-Grade Prostatic Intraepithelial Neoplasia (HGPIN), and Prostate Adenocarcinoma (PRAD). Methods: This was a cross-sectional study using three groups of samples, namely BPH, HGPIN, and PRAD. Tissue samples were obtained from TURP Action. The expression of miR-155 was analyzed using real-time qPCR and calculated using the Livak method. The expression of SOCS1 mRNA was analyzed using reverse transcriptase PCR. The macrophage pan-marker, anti-CD68 monoclonal antibody (MoAb), was used to detect macrophage population in tissues by immunohistochemistry. Results: The expression of miR-155 was higher in HGPIN than BPH and PRAD (p=0.14). The expression of SOCS1 mRNA in HGPIN was the lowest among the three samples (p=0.96). There was a negative correlation between miR-155 and SOCS1 mRNA (p=0.02). There was a significant increase in the percentage of the macrophage population in HGPIN (6.03 percent) compared to BPH (0.89 percent) with p=0.00. Conclusion: In this study, there were changes in the percentage of macrophage and miR-155 in HGPIN. The variation in miR-155 expression and the percentage of the macrophage may be caused by epigenetic changes. Therefore, further research is needed to validate these results and understand the possibility of being a biomarker in precancerous disease of the prostate. Keywords: Prostatic Intraepithelial Neoplasia, miR-155, Macrophage

Efek Sitotoksik Madu Dan Silver Dressing Terhadap Sel Fibroblas Dalam Media Tinggi Glukosa: Studi In Vitro Januar Rizqi; Denny Agustiningsih; Dwi Aris Agung; Nur Arfian
Jurnal Keperawatan Respati Yogyakarta Vol 6 No 2 (2019): MAY 2019
Publisher : Universitas Respati Yogyakarta

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.35842/jkry.v6i2.316

Penyembuhan luka diabetes merupakan proses yang unik dan kompleks. Sejumlah dressing dikembangkan untuk mengetahui manfaat yang diharapkan meningkatkatkan proses penyembuhan. Penelitian in vivo maupun in vitro madu dan silver menunjukan hasil yang berbeda. Diperlukan penelitian lebih lanjut aktifitas sitotoksik madu dan silver terhadap sel fibroblas dalam media tinggi glukosa. Penelitian inibertujuan untuk mengetahui apakah madu dan silver bersifat sitotoksik terhadap sel fibroblast dalam media tinggi glukosa. Jenis penelitian ini adalah kuasi eksperimental dengan post test only desain. Kultur sel fibroblast di uji sitotoksik dengan meggunakan metode MTT Assay secara in vitro. Kelompok penelitian dibagi menjadi kelompok madu dengan konsentrasi 6%, 3% 1.5% dan kelompok Silver. Silver memiliki efek sitotoksik terhadap sel fibroblas dengan nilai penghambatan sebesar 100%. Madu dengan konsentrasi 6% dan 3% memiliki nilai penghambatan lebih dari 50%. Madu konsentrasi 1,5% menujukan proses penghambatan kurang dari 50% dan meningkatkan proses priliferasi sel fibroblas dalam media tinggi glukosa. Madu memiliki aktifitas sitotoksik yang lemah terhadap sel fibroblas dan dapat meningkatkan proliferasi sel, sedangkan silver memiliki aktifitas sitotoksik yang kuat terhadap sel fibroblast.

Role of nuclear factor-κB (NFκB) in microglial polarization in correlation with neuroinflammatory mechanism at the hippocampal cornu ammonis (CA) 1 region after acute and chronic phase of global ischemic brain injury in rats Wibisono, Dian Prasetyo; Nur Arfian; Fauziyatul Munawaroh; Dwi Cahyani Ratna Sari
Indonesian Journal of Biomedicine and Clinical Sciences Vol 57 No 3 (2025)
Publisher : Published by Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/inajbcs.v57i3.12757

Ischemic brain injuries can result in hippocampal injury due to its vulnerability to ischemia, specifically the CA1 region. Ischemic injury to this region alters nerve cells, synapses, and non-neural hippocampal tissue and causes hippocampal sclerosis. This injury could be mediated by microglia via the neuroinflammation pathway. However, the neuroinflammatory mechanism underlying hippocampal ischemic injury is still unclear. This study aimed to investigate the role of NF-κB in microglia polarization which affects the hippocampal area after ischemic injury. We conducted a quasi-experimental study, using 24 male Sprague Dawley rats aged 4 wk old and weighing 100 g. The rats were grouped into 4 different groups (CL1 as acute, CL3 as subacute, CL7 as chronic, and SO as control groups) and performed bilateral common carotid artery ligation to induce global ischemic injury in the brain. The difference in microglial activation was tested using immunohistochemistry for CD68. Moreover, polymerase chain reaction (PCR) was utilized to assess mRNA expression differences in IL1β, IL6, TNFα, and NF-κB. An increase in the number of positive CD68 fraction areas in CL1, CL3, and CL7 compared to the SO group (p=0.002) was shown after bilateral common carotid artery ligation. Such ligation also induced a significantly higher mRNA expression of IL1β (p=0.004), IL6 (p=0.028), TNFα (p=0.028), and NF-κB (p=0.002) in the CL1, CL3, and CL7 groups, compared to the SO group. In conclusion, NF-κB is the key player in hippocampal injury in the CA1 region following ischemic event by differentiating microglia into M1 phenotype form and initiates the neuroinflammatory cascade via IL1β, IL6, and TNFα in all phases.

Co-Authors Danarto Danarto Denny Agustiningsih Desby Juananda Didik Setyo Heriyanto Djoko Prakosa2, Dwi Aris Agung Dwi Cahyani Ratna Sari Fauziyatul Munawaroh Indwiani Astuti Januar Rizqi Mansyur Romi Mawaddah Ar-Rochmah Muhammad Mansyur Romi Rachma Greta Putri Sari Eka Pratiwi Sofia Mubarika Haryana Wibisono, Dian Prasetyo

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