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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.
Combination of Aerobic Exercise and Continuous Environmental Enrichment Improves Adult Male Rats’ Spatial Memory: Study on Hippocampal Insulin Like Growth Factor 1 (IGF-1) and Fibroblast Growth Factor 2 (FGF-2) Expression Sophie Yolanda; Sri Redjeki; Trinovita Andraini; Dewi Irawati Soeria Santoso; Nurhadi Ibrahim; Rena Mailani
The Indonesian Biomedical Journal Vol 11, No 2 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i2.731

Abstract

BACKGROUND: Memory declines with the progression of age through the neurodegeneration process. Aerobic exercise and environmental enrichment can delay neurodegeneration by improving neuroplasticity via expression of insulin like growth factor 1 (IGF-1), fibroblast growth factor 2 (FGF-2) and other proteins. Combination treatment of aerobic exercise and continuous environmental enrichment and their effect on the expression of IGF-1 and FGF-2 which were expected to improve memory function has not been studied previously. Thus, this study aimed to observe it.METHODS: This is an experimental research using 24 male Wistar rats (Rattus norvegicus, 300-400 g, age 7-8 months) divided randomly into 4 groups: control (C), aerobic exercise (A), continuous (EE), and combination of aerobic exercise and continuous environmental enrichment (A-EE). At the end of an 8-week treatment, rats were sacrificed, and an enzyme-linked immunosorbent assay (ELISA) examination was performed to assess hippocampal IGF-1 and FGF-2 levels.RESULTS: In the 8th week, A-EE group showed the best improvement in rats’ spatial memory (47.84±10.6 %) followed by EE group (45.03±4.1 %), A group (38.61±3.8 %), and C group (22.76±7.12 %). However, A-EE group’s hippocampal IGF-1 (16.21±7.56 ng/mg protein) and FGF-2 (1.29±0.57 ng/mg protein) expression were not higher than other groups.CONCLUSION: Improvement in memory function in the combination group is a result of induction of various growth factors’ expression in the hippocampus, including IGF-1 and FGF-2, but the primary pathway of memory function improvement may be from other growth factors.KEYWORDS: spatial memory, aerobic exercise, environmental enrichment, hippocampus, IGF-1, FGF-2
EKSTENSI DAN INVASI INTRAKRANIAL TUMOR KULIT KEPALA: TANTANGAN DIAGNOSIS DAN TATALAKSANA Sophie Yolanda; Tiara Aninditha; Henry Riyanto Sofyan; Rahmad Mulyadi
NEURONA Vol 39 No 2 (2022): Vol 39 No 2 (2022)
Publisher : PERDOSNI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52386/neurona.v39i2.312

Abstract

Scalp tumors are quite rare, only 1-2% are malignant and have a tendency for intracranial extension and invasion. This extension can lead to various neurological complications, such as cancer pain, increased intracranial pressure (ICP), and other neurological deficits. A 37-year-old woman presented with decreased consciousness since 2 days earlier. The patient had a history of lump on the top of her head since 4 years, repeated 3 times after resection without previous treatment. On the third recurrence, the tumor was enlarged until it some part of the tumor can be seen depressed against the skull and this part was painful. The pain worsened throughout the entire head accompanied by visual field disturbance of right inferior homonymous quadranopia, right central facial nerve paresis, and right hemiparesis. Contrast head CT scan revealed lobulated heterogeneous lesion in the parietooccipital region, extending to the extraaxial and intracerebral, accompanied by vasogenic edema with destruction of the parietal and occipital bones. The result of histopathology is trichilemmal carcinoma. The patient received morphine drip therapy 10mg/24 hours for the cancer pain, which was then replaced with its patch equivalent dose, dexamethasone 2x10mg IV tapering off gradually according to the clinical condition, gabapentin 2x300mg, and wholebrain radiotherapy (WBRT) 30 Gy in 10 sessions. The patient was discharged in conscious condition and her pain resolved to mild pain. Keywords: cancer pain, increased intracranial pressure, intracranial invasion, scalp tumor
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.