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All Journal Universa Medicina Eksakta : Berkala Ilmiah Bidang MIPA
Sophie Yolanda
Department of Physiology Faculty of Medicine, Universitas Indonesia, Jakarta
Agriculture, Biological Sciences & Forestry Astronomy Biochemistry, Genetics & Molecular Biology Chemical Engineering, Chemistry & Bioengineering Chemistry Civil Engineering, Building, Construction & Architecture Computer Science & IT Energy Engineering Environmental Science Health Professions Immunology & microbiology Materials Science & Nanotechnology Mathematics Mechanical Engineering Medicine & Pharmacology Public Health

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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.
LOW VITAMIN B12 DIET INCREASES LIVER HOMOCYSTEINE LEVELS AND LEADS TO LIVER STEATOSIS IN RATS Sianipar, Imelda Rosalyn; Ujianti, Irena; Yolanda, Sophie; Jusuf, Ahmad Aulia; Kartinah, Neng Tine; Amani, Patwa; Murti, Krishna Aditya; Soeria Santoso, Dewi Irawati
Universa Medicina Vol 38, No 3 (2019)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (821.825 KB) | DOI: 10.18051/UnivMed.2019.v38.194-201

Abstract

Background Nonalcoholic fatty liver disease (NAFLD) is one of the most widespread chronic liver diseases, caused by the development of insulin resistance. One of the mechanisms involved is a disturbance in insulin signaling by certain toxic substances that interact with one of the proteins responsible for the insulin signaling pathway. Increased homocysteine level, upon disruption of the methionine pathway, is associated with insulin resistance. The aim of this study was to evaluate the effect of hyperhomocysteinemia and insulin resistance (HOMA-IR level) induced by dietary vitamin B12 restriction on liver steatosis. Methods A study of laboratory experimental design was conducted involving 18 male Sprague Dawley rats (age 36-40 weeks, BW 300-350 g), that were randomly divided into 3 groups: control, 8-week treatment, and 16-week treatment. Standard AIN-93 diet was administered to the control group, whereas rats in the treatment groups were fed vitamin B12 deficiency-AIN-93M. At the end of treatment, liver homocysteine levels were determined by ELISA, HOMA-IR values were calculated, and steatosis degree of the liver was determined histologically. Statistical analysis was performed using independent t-test. Results A significant increase in liver homocysteine levels was found between the control and both the 8- and 16-week treatment groups (p<0.001). HOMA-IR levels were significantly higher in both treatment groups compared to controls (p<0.001). The area of liver steatosis in both treatment groups was significantly larger than that of the control group (p<0.001). Conclusion Increased homocysteine levels due to dietary vitamin B12 deficiency induces liver steatosis due to insulin resistance in rats.
Learning and Memory Impairment in High Fat Diet Induced Obesity Ariani, Citra; Ibrahim, Nurhadi; Yolanda, Sophie
EKSAKTA: Berkala Ilmiah Bidang MIPA Vol. 26 No. 01 (2025): Eksakta : Berkala Ilmiah Bidang MIPA (E-ISSN : 2549-7464)
Publisher : Faculty of Mathematics and Natural Sciences (FMIPA), Universitas Negeri Padang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24036/eksakta/vol26-iss01/483

Abstract

Obesity is a manifestation of abnormal fat accumulation which can lead to impairment in several organs, including the brain. Neuroinflammation is considered the cause of cell death as well as reactive oxygen species in hippocampal neuron cells. It results in disturbance of memory forming process. Impaired learning and memory function affects a person's ability to carry out daily tasks and lower quality of life over time, so they should be circumvented with preventive, curative, and rehabilitative measures. The understanding of the pathological mechanisms of obesity-induced memory impairment based on the changes at molecular levels is imperative for an effective management. We collected and reviewed research articles to summarize the pathological mechanisms. Twenty studies were included in this review in terms of signaling pathway, molecular markers in brain and changes in memory and behavior pattern. It is showed that memory changes in obesity could be resulted from inflammation, impaired neurogenesis and cell senescence via various mechanisms and pathways. In conclusion, the understanding of the pathomechanisms in obesity-induced memory impairment aids to its the prevention and treatment.
Co-Authors Ahmad Aulia Citra Ariani, Citra Endang W. Bachtiar Handayani, Astri Imelda Rosalyn Sianipar Indra Kusuma Irena Ujianti Murti, Krishna Aditya Neng Tine Kartinah Almuktabar Nurhadi Ibrahim Patwa Amani, Patwa Radiana D. Antarianto Ria Kodariah Santoso, Dewi Irawati Soeria Stefanus, Robert Trinovita Andraini