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Centella asiatica ethanol extract increases hippocampal brain derived neurotrophic factor in male Wistar rats Handayani, Astri; Yolanda, Sophie; Kodariah, Ria
Universa Medicina Vol 37, No 2 (2018)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2018.v37.143-149

Abstract

BackgroundSynaptic plasticity, which primarily takes place in the hippocampus, is the molecular basis of long- term memory formation. Brain derived neurotrophic factor (BDNF), a member of the neurotrophin family, plays a significant role in synaptic plasticity and memory formation. When BDNF is released, it binds to its receptor and activates various intracellular signal transduction pathways leading to synaptic plasticity. Several methods to improve memory function in humans have been studied, one of which is the use of herbal compounds, such as Centella asiatica (CeA), an herbaceous plant that has been used for improving memory. This study aims to examine the effects of CeA ethanol extract on BDNF protein expression in the CA1 hippocampal region in adult male rats.MethodsA randomized experimental design was performed involving 18 adult male Wistar rats. The rats were randomized into three groups: one control/distilled water group and two groups treated with doses of CeA ethanol extract of 300 mg/kgBW (CeA300) and 600 mg/kgBW (CeA600), respectively. CeA ethanol extract was administered orally for 28 consecutive days with weekly weight-adjusted dose. After 28 days, the rats were decapitated, and the hippocampus was isolated from the brain. BDNF protein expression was assessed using immunohistochemistry. Data was analyzed using Kruskal-Wallis test and continued with post-hoc analysis. ResultsThere was a significant increase in BDNF protein expression in the CeA600 group compared to the control group (p<0.001). ConclusionAdministration of CeA ethanol extract increased BDNF protein expression in the CA1 hippocampal region of adult male rats.
Analysis Expression of ZIP1 and Caspase-3 Protein in Adenocarsinoma of the Prostate Septiawan, Aditya D; Kodariah, Ria; Saraswati, Meilania
Makara Journal of Health Research Vol. 20, No. 1
Publisher : UI Scholars Hub

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Abstract

Background: Carcinogenesis of adenocarcinoma of the prostate occurs due to dysregulation of zinc level within the cells. Intracellular zinc molecules influx is regulated by a transporter protein ZIP1, whose non-presence is predicted to inhibit apoptosis, thus leads to the development of prostate adenocarcinoma. Methods: This study was aimed to analyse the correlation of ZIP1 and Caspase-3 expression in prostate adenocarcinoma on its grading as represented by Gleason Score. This was a cross-sectional, retrospective analytical study on 31 Formalin-fixed, paraffin-embedded tissue that meets inclusion criteria. The specimen was stained using the immune-histochemistry technique for ZIP1 and Caspase-3. Protein expression of each case was counted using ImageJ analysis. Gleason score was acquired as secondary data from the cases' reports. The correlation of their expression with respect to Gleason score was analysed with Pearson's correlation using SPSS 11.5. Results: Mean expression level of ZIP1 and Caspase-3 in prostate adenocarcinoma were 35% and 33%, respectively. There was a significantly positive correlation between ZIP1 and Caspase-3 expression (r = 0.379; p = 0.018). However, their correlation was stronger in intermediate-grade group (r = 0.73; p = 0.01) and the correlation was much weaker in high-grade group (r = 0.04; p = 0.48). Conclusions: There was a positive correlation between ZIP1 and Caspase-3 expression in prostate adenocarcinoma.
T HELPER 17 (Th17) AND REGULATORY T (Treg) CELLS PROFILE IN TYPE-2 DIABETES MELLITUS (T2DM) DWIKARJANTI, INDRANITA; KRISNAMURTI, DESAK GEDE BUDI; KODARIAH, RIA
BIOMA : Jurnal Ilmiah Biologi Vol. 14 No. 1 (2025): April 2025
Publisher : LPPM Universitas PGRI Semarang

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.26877/bioma.v14i1.1208

Abstract

One of metabolic disorder disease is Type 2 Diabetes mellitus (DM), leading to increased glucose, cholesterol, and lipid levels in the blood. Type 2 DM results in insulin resistance within the body. Glycolysis, oxidative phosphorylation, and fatty acid are the three main metabolic pathways which provide energy for T cells. T cells will ploriferate, differentiate and become active into T Helper-17 and T regulator (Treg) cells because of these pathways. The profile of TH-17 cells and Treg cells in type 2 diabetes will be opposite in terms of the number of their populations caused by metabolic disorders in the body. Type 2 diabetes make an immunology response with increasingly number of TH-17 cells, while lack of Treg cells. Many studies have shown that diabetes mellitus as a metabolic disease effect populations of T Helper-17 and regulatory T cells. Glycolysis is the main energy metabolism becomes important factor that stimulate the proliferation and differentiation of Th-17 cells. The energy produced from this metabolism is in the form of ATP, which is the result of glucose synthesis using the Glucose transporter (GLUT). Glucose transporters (GLUT-1) are most dominantly expressed by Th-17 cells and Treg cells. Metabolic disorder causes an imbalance in the population of TH-17 cells with Treg cells. This review will explain the profiles of TH-17 and regulatory T cells in Diabetes mellitus and their relationship with body metabolism disease.
VEGF mRNA Expression in Epithelial Ovarian Cancer: Correlation with rs699947 Gene Variant Prameswari, Yuda Nabella; Suryandari, Dwi Anita; Sukmawati, Dewi; Yunaini, Luluk; Kodariah, Ria
Journal of Biomedicine and Translational Research Vol 11, No 2 (2025): August 2025
Publisher : Faculty of Medicine, Universitas Diponegoro

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14710/jbtr.v11i2.26156

Abstract

Background: Angiogenesis is the formation of new blood vessels, is crucial for cancer growth and metastasis, including in epithelial ovarian cancer (EOC). Vascular Endothelial Growth Factor (VEGF) regulates angiogenesis, and its elevated mRNA expression is linked to poor prognosis in cancer. Genetic variations, such as the rs699947 polymorphism in the VEGF gene, can affect VEGF expression and contribute to cancer progression.Objective: The primary aim of this study is to examine the distribution of the VEGF rs699947 polymorphism and its correlation with VEGF mRNA expression levels in patients with low-grade and high-grade EOC at Dr. Cipto Mangunkusumo Hospital, Indonesia.Methods: This research is a cross-sectional analysis involving 65 normal female whole blood samples and a total of 80 ovarian cancer biopsy samples, including 15 ovarian cysts as expression calibrators, along with 36 low-grade and 29 high-grade EOC samples. The distribution of genotypes and alleles of the VEGF rs699947 polymorphism was assessed through ARMS PCR analysis, while VEGF mRNA expression was quantified using real-time qPCR.Results: Significant differences were observed in both genotype (p<0,01) and allele (p=0,000) distributions between the normal and cases group. The relative mRNA expression of VEGF was significantly elevated in both low-grade and high-grade EOC. Individuals with the homozygous VEGF rs699947 AA genotype exhibited the highest mRNA expression compared to other genotypes. In contrast, individuals carrying the CC genotype showed the lowest correlation with VEGF mRNA expression in both low-grade and high-grade EOC.Conclusion: This study shows that the A allele of VEGF rs699947 is correlated with increased VEGF mRNA expression in EOC patients, particularly in those with the AA genotype. Conversely, the C allele may offer a protective effect against EOC, as the CC genotype is linked to lower VEGF mRNA expression. Genetic screening for VEGF rs699947 could facilitate early detection and inform targeted therapeutic strategies.
Analysis of H3k27me3 Expression in Malignant Peripheral Nerve Sheath Tumor (MPNST) and Other Spindle Cell Sarcoma Mimicking MPNST Yordana, William; Evelina, Evelina; Kodariah, Ria
Majalah Patologi Indonesia Vol. 32 No. 3 (2023): MPI
Publisher : Perhimpunan Dokter Spesialis Patologi Anatomik Indonesia (PDSPA)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.55816/mpi.v32i3.585

Abstract

Malignant Peripheral Nerve Sheath Tumor (MPNST) is a type of spindle cell sarcoma with approximately 5% of all sarcomas. Its diagnosis is challenging due to the absence of specific immunohistochemical markers. Recently, H3K27me3 was discovered as a potential specific immunohistochemical marker to differentiate MPNST from other sarcomas and distinguish between low and high-grade MPNST. Therefore, this research aims to investigate the use of the H3K27me3 as a potential specific marker for Malignant Peripheral Nerve Sheath Tumor (MPNST). A cross-sectional analysis was conducted on 50 cases of sarcomas, including 13 MPNST, 14 synovial sarcomas, 13 dermatofibrosarcoma protuberans (DFSP), and 10 leiomyosarcomas originating from the Department of Anatomical Pathology, Faculty of Medicine, Universitas Indonesia, Cipto Mangunkusumo Hospital (FMUI-CMH) from January 2013 to December 2021. H3K27me3 images were obtained and categorized as complete loss when more than 95% of the tumor cells showed loss of nuclear staining. The results found in MPNST showed a loss of H3K27me3 expression, which is statistically significant compared to other sarcomas mimicking MPNST (p=0.021), indicating its potential as a diagnostic marker. There is a difference in the expression of H3K27me3 between the high and low-grade MPNST but it is not statistically significant (p=0.105). This showed that H3K27me3 loss of expression can be used to diagnose MPNST, especially high-grade MPNST, and differentiate it from other sarcomas mimicking MPNST.