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All Journal Jurnal Ilmu Kedokteran (Journal of Medical Science) Majalah Kedokteran Bandung Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Indonesian Journal of Biotechnology Mutiara Medika: Jurnal Kedokteran dan Kesehatan Jurnal Pendidikan Kedokteran Indonesia: The Indonesian Journal of Medical Education Majalah Kesehatan Pharmamedika Muhammadiyah Journal of Geriatric Indonesian Archives of Biomedical Research (InABR)
Dwi Cahyani Ratna Sari
Departement Of Anatomy, Faculty Of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia
Biochemistry, Genetics & Molecular Biology Dentistry Health Professions Immunology & microbiology Materials Science & Nanotechnology Medicine & Pharmacology Neuroscience Public Health

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Journal : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

 1 
Neuroprotective effect of vitamin D3 toward apoptosis induced by ethanol in CA1 pyramidal cells of rat hippocampus Dwi Cahyani Ratna Sari, Junaedy Yunus Djoko Prakosa
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 44, No 01 (2012)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1610.308 KB)

Abstract

As an antioxidant, Vitamin D3 can protect neurons from damage caused by oxidative stress.Ethanol is known to have neurotoxic effects by inducing an increase in oxidative stress. One ofthe brain regions that is most sensitive to neurotoxic effects induced by ethanol is hippocampus,especially its CA1 region. This study was aimed to determine the neuroprotective effects ofvitamin D3 in preventing the apoptosis in CA1 hippocampal pyramidal cells induced by ethanol.Fifteen male Wistar rats (Rattus norvegicus) were randomly divided into three groups. The controlgroup was given daily normal saline solution intraperitoneally. The ethanol group was given20% ethanol solution at a dose of 3 g/kg BW/day intraperitoneally. The vitamin D3 group wasgiven vitamin D3 1 μg/kg BW/day in 20% ethanol solution at a dose of 3 g/kg BW/dayintraperitoneally. After 30 days, the rats were sacrificed, their brains were perfused with PBSfollowed by fixative and the hippocampus was dissected for histological preparations.Immunohistochemical staining for caspase was performed. Percentage of apoptotic CA1hippocampal pyramidal cells was calculated. The results showed there was no significant difference(p> 0.05) on the total number of pyramidal cells between the control group (20.52 ± 1.31), theethanol group (19.02 ± 1.60), and the vitamin D3 group (21. 06 ± 0.70) per field of view.However there was a significant increase (p<0.05) in the percentage of apoptotic CA1hippocampal pyramidal cells in in the ethanol group (16.09 ± 0.67%) compared to the controlgroup (10.60 ± 0.95%). Vitamin D3 significantly (p<0.05) prevented an increase in the percentageof apoptotic CA1 hippocampal pyramidal cells in the vitamin D3 group (10.82 ± 0.64%). Inconclusion, vitamin D3 had a neuroprotective effect to prevent an increase in apoptosis in CA1hippocampal pyramidal cells to the neurotoxic effects induced by ethanol.
Neuroprotective effect of vitamin D3 toward apoptosis induced by ethanol in CA1 pyramidal cells of rat hippocampus Junaedy Yunus Djoko Prakosa Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 44, No 01 (2012)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1610.308 KB)

Abstract

As an antioxidant, Vitamin D3 can protect neurons from damage caused by oxidative stress.Ethanol is known to have neurotoxic effects by inducing an increase in oxidative stress. One ofthe brain regions that is most sensitive to neurotoxic effects induced by ethanol is hippocampus,especially its CA1 region. This study was aimed to determine the neuroprotective effects ofvitamin D3 in preventing the apoptosis in CA1 hippocampal pyramidal cells induced by ethanol.Fifteen male Wistar rats (Rattus norvegicus) were randomly divided into three groups. The controlgroup was given daily normal saline solution intraperitoneally. The ethanol group was given20% ethanol solution at a dose of 3 g/kg BW/day intraperitoneally. The vitamin D3 group wasgiven vitamin D3 1 μg/kg BW/day in 20% ethanol solution at a dose of 3 g/kg BW/dayintraperitoneally. After 30 days, the rats were sacrificed, their brains were perfused with PBSfollowed by fixative and the hippocampus was dissected for histological preparations.Immunohistochemical staining for caspase was performed. Percentage of apoptotic CA1hippocampal pyramidal cells was calculated. The results showed there was no significant difference(p> 0.05) on the total number of pyramidal cells between the control group (20.52 ± 1.31), theethanol group (19.02 ± 1.60), and the vitamin D3 group (21. 06 ± 0.70) per field of view.However there was a significant increase (p<0.05) in the percentage of apoptotic CA1hippocampal pyramidal cells in in the ethanol group (16.09 ± 0.67%) compared to the controlgroup (10.60 ± 0.95%). Vitamin D3 significantly (p<0.05) prevented an increase in the percentageof apoptotic CA1 hippocampal pyramidal cells in the vitamin D3 group (10.82 ± 0.64%). Inconclusion, vitamin D3 had a neuroprotective effect to prevent an increase in apoptosis in CA1hippocampal pyramidal cells to the neurotoxic effects induced by ethanol.
Prefrontal cortex cell proliferation of adult rats after chronic stress treated with ethanolic extract of Centella asiatica (L) Urban. Yuniasih Mulyani Jubeliene Taihuttu; Ginus Partadiredja; Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 1 (2016)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1127.045 KB) | DOI: 10.19106/JMedSci004801201601

Abstract

The decrease of proliferation level of cells in several regions of adult brain is found afterstress exposure. One of such area is prefrontal cortex. Herbal medicine as antistresshas been used widely. Centella asiatica (L) Urban extract was reported to have potentcompounds to increase brain function. The objective of this study is to investigate theeffects of ethanolic extract C. asiatica on cell proliferation of the adult prefrontal cortexin rats (PFC) after chronic stress. Adult male Sprague-Dawley rats, weighing 260-390g were randomly assigned into six experimental groups, with five rats per group, i.e.Group 1 as nomal control without chronic stress, Group 2 as stress control, Group 3 aspositive control given fluoxetine, Group 4-6 as treatment groups given 150; 300 and 600of ethanolic extrac C. asiatica, respectively. Extract were administered orally to the ratsfollowing a period of restraint duration of 6 hours/day for 21 days. Bromodeoxyuridine(BrdU) immunohistochemistry was used to label the proliferated cells. Physical fractionatormethod was used to estimate the total number of proliferated cells. One-way analysis ofvariance (ANOVA) followed by Tukey post hoc test was used to evaluate the differencebetween groups. BrdU-labeled cells on medial prefrontal cortex were as follows:1715.3±1345.1 (Group 1), 2659.2±2250.6 (Group 2), 4077.4±2415.3 (Group 3),1784.1±908.3 (Group 4), 3056.6±4263.3 (Group 5), and 2153.4±2259.4 (Group 6).No significance difference between groups was observed (p>0.05). In conclusion, theadministration of ethanolic extract of C. asiatica does not influence cell proliferation onprefrontal cortex of rats after chronic stress.
Prolonged Kidney Ischemia-Reperfusion Injury Associates with Inflammation, Vascular Remodelling, and Myofibroblast Formation Nur Arfian*; Hilma Kholida Ats-tsani; Pratiwi Indah Sayekti; Dwina Agrila Lakabela; Amelia Amelia; Toni Febriyanto; Hana Rutyana Putri Antonio; Dian Prasetyo Wibisono; Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 50, No 1 (2018)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1436.153 KB) | DOI: 10.19106/JMedSci005001201801

Abstract

Prolonged kidney ischemia-reperfusion injury (IRI) is the important risk factor for leading to chronic kidney disease (CKD). Persistent hypoxia and inflammation are considered as the main pathogenesis of chronic injury, followed by myofibroblast expansion and fibrosis process. Tubular injury, cell proliferation, and vasoconstriction, as acute compensatory responses, are restored in chronic phase. The aim of the study was to investigate the relation between inflammation, vascular remodeling, and myofibroblast formation as response to ischemia injury after prolonged kidney ischemia-reperfusion (I/R). Fifteen male Swiss mice aged 3-4 months were used as kidney I/R injury model after bilateral pedicle renal clamping. Rats were divided into 3 groups with five rats in each group i.e. control group (sham operation/SO), acute I/R model (IR1), and chronic I/R model (IR12). PAS staining was used for scoring tubular injury. Fibrosis was assessed using sirius red and a-SMA immunostaining for myofibroblast expansion. PCNA and CD68 immunostaining were used for identifying cell proliferation and macrophage infiltration. RT-PCR was conducted for assessing MCP-1, HIF-1a, and ppET-1 expression, which were quantified using ImageJ software. Data were analyzed using one way ANOVA and Kruskal-Wallis test with significance level of p<0.05. Significantly increase of tubular injury score (p<0.001) and PCNA positive cell (p<0.001) in IR1 group compared to SO were observed, otherwise HIF-1a of IR12 enhanced (p<0.05). Macrophage cell count (p<0.01) and MCP-1 expression (p<0.05), were significantly increase in IR1 and IR12 injury, compared to SO. Wall thickness of arteries was significantly increase (p<0.05) as well as decrease of vascular lumen area (p<0.05), followed by enhancement of ppET-1 expression (p<0.01) in IR1 group and restored significantly (p<0.05) in IR12 group. Fibrosis fraction-area and myofibroblast expansion were significantly increase gradually from IR1 to IR12 injury (p<0.01). In conclusion, prolonged kidney I/R injury induces the sustainability of hypoxia and inflammatory response, which promotes myofibroblast formation, and decrease the response of vascular remodelling. 
Ethanolic extract of the Centella asiatica (L.) Urb. leaf decreases cerebellar brain-derived neurotrophic factor (BDNF) levels in rats after chronic stress Dwi Cahyani Ratna Sari; Desby Juananda; Mawaddah Ar-Rochmah; Muhammad Mansyur Romi; Nur Arfian
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 50, No 2 (2018)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (770.994 KB) | DOI: 10.19106/JMedSci005002201801

Abstract

Chronic stress produces glucocorticoid-induced neurotoxicity that may lead to alterations of the brain-derived neurotrophic factor (BDNF) concentration in the brain. Cerebellum is known to be severely affected by glucocorticoids-associated oxidative damage. Centella asiatica (L.) Urb. may protect neurons from oxidative damage. This study aimed to investigate the effect of ethanolic extract of C. asiatica (L.) Urb. leaf on the rat cerebellar BDNF levels following stress. Twenty young-adult male Sprague Dawley rats were randomly assigned into four experimental groups. The stress control group received aquadest, and the other groups were treated with different doses of the C. asiatica (L.) Urb. extract i.e 150 (CeA150), 300 (CeA300) and 600 (CeA600) mg/kg body weight/day orally, respectively and followed by chronic footshock stress for 28 days. Upon completion of the experimental period, all animals were sacrificed and the cerebellar was isolated. The BDNF levels from the cerebellar tissue lysate was measured using ELISA. The mean BDNF levels of the cerebellar tissue in the stress control, CeA150, CeA300 and CeA600 groups were 1217.10±301.40; 771.46±241.45; 757.05±268.29; and 627.00±246.02 pg/mL, respectively. Post-hoc analysis showed a significant difference between the control and treatment groups (p< 0.05). In conclusion, the ethanolic extracts of the C. asiatica (L.) Urb. leaf decrease the cerebellar BDNF levels in rats after chronic stress.
Increased blood-brain barrier permeability correlate with microglial activation at hippocampal CA1 region in acute and chronic bilateral common carotid artery ligation in rats Dian Prasetyo Wibisono; Nur Arfian; Handoyo Pramusinto; Fauziyatul Munawaroh; Yeshua Putra Krisnugraha; Daniel Agriva Tamba; Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 54, No 2 (2022)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19106/JMedSci005402202201

Abstract

Inflammatory processes might play a key role in the pathogenesis of post-stroke epilepsy. The activation of microglia and release of vascular cell adhesion molecule-1 (VCAM1) might induce blood-brain barrier (BBB) disintegration. However, the influence of such pathomechanisms in the generation of post-stroke epilepsy is still not clear. We investigated whether cerebral ischemia exerts effects on inflammation in the hippocampus by measuring the hippocampal injury score, expression of a microglial marker, and expression of VCAM1 in rats. A total of 24 Sprague Dawley rats were randomized into four groups with 6 rats in eachgroup i.e. sham operation (SO) as control, carotid ligation 1 (GCL1) as an acute model, carotid ligation 3 (GCL3) as a subacute model, and carotid ligation 7 (GCL7) as a chronic model. Immunostaining for microglia marker (CD68) was measured in rat brain tissue sections. The VCAM1 expression was evaluated by reverse transcription-polymerase chain reaction (RT-PCR). Cerebral ischemia increased the amount of microglial immunostaining and expression of VCAM1. The hippocampal injury score and microglial immunopositivity were significantly correlated with the duration of brain ischemia. We conclude that cerebral ischemia is correlated with neuroinflammatory reaction and disturbance of BBB permeability, and the correlation of those molecular impairments with the generation of post-stroke epilepsy remains to be elucidated.
Co-Authors Agustiningsih, Denny Amelia Amelia Anggi Setiorini Budi Iman Santoso Daniel Agriva Tamba Desby Juananda Desby Juananda Dian Prasetyo Wibisono Djoko Prakosa2, Dwina Agrila Lakabela Fauziyatul Munawaroh Ginus Partadiredja Ginus Partadiredja Hana Rutyana Putri Antonio Handoyo Pramusinto Hilma Kholida Ats-tsani M. Mansyur Romi Mansyur Romi Mawaddah Ar-Rochmah Mawaddah Ar-Rochmah Muhammad Mansyur Romi Muhammad Mansyur Romi Muhammad Mansyur Romi Muhammad Mansyur Romi Nanang Wiyono Nur Arfian Nur Arfian Nur Arfian Nur Arfian Nuring Pangastuti, Nuring Ova Emilia Pratiwi Indah Sayekti Reza Satria Pratama Reza Satria Pratama, Reza Satria Riky Setyawan Soedjono Aswin Soedjono Aswin Sri Suharmi, Sri Toni Febriyanto Wiwit Ananda Wahyu Setyaningsih Yenni Zulhamidah, Yenni Yeshua Putra Krisnugraha Yuniasih Mulyani Jubeliene Taihuttu