Biomolecular Aspects of Schizophrenia

Wulandari, Patricia

doi:10.32539/bsm.v3i2.88

Cited by 2 publications

(3 citation statements)

References 11 publications

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“…11 Apoptosis in prefrontal neuronal cortex cells will cause cell population decline, and definitely it will be followed by a decrease in receptors, especially serotonin receptors. 1,2 The decrease in these receptors send a negative feedback mechanism related to serotonin production in the raphe nucleus. This will cause a decrease in serotonin production.…”

Section: Resultsmentioning

confidence: 99%

“…This has implications for the development of various antidepressant drugs that work to increase serotonin levels, by inhibiting serotonin reuptake. [1][2][3] However, management with antidepressants is still believed to be not optimal, there are still various problems that have not been able to be solved only by increasing serotonin levels in the brain. Therefore, it is necessary to do further exploration to find out other possible pathophysiology of depressive disorders.…”

Section: Introductionmentioning

confidence: 99%

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Neuronal Cell Death Induces Depressive Disorder in Rats Depression-Like Behaviors Caused by Chronic Stress

Hidayat

Saleh

Parisa

2020

SciPsy

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Abstract Introduction Depression is believed to be a disorder in which an increase in serotonin activity in the brain. This has implications for the development of various antidepressant drugs that work to increase serotonin levels, by inhibiting serotonin reuptake. However, management with antidepressants is still believed to be not optimal, there are still various problems that have not been able to be solved only by increasing serotonin levels in the brain. Therefore, it is necessary to do further exploration to find out other possible pathophysiology of depressive disorders. This study intended to explore the role of apoptosis of neuronal cells in the prefrontal cortex to answer the hypothesis that depression was not only caused by increased serotonin levels but also there was a role of dead neuronal cells in the prefrontal cortex which will trigger the body's homeostatic efforts to compensate by increasing serotonin levels. Methods A total of 30 male Wistar rats (200 ± 20 g) were obtained from Eureka Research Laboratory (Palembang, Indonesia). Experimental animals were placed in cages under controlled conditions (12 hours of light / dark cycles with temperatures of 22 ± 1˚C and humidity of 40-60%), fed and drank ad libitum. Experimental animals with depression model were induced using Chronic Mild Stress (CMS). CMS procedures were performed with mild stressors such as repeated cold stress (4 ° C), space reduction in the homecage, changed cages and social interaction with other animals of the CMS group. To assess wether animal were being depression or not, the animal were tested using Forced Swimming Test (FST). After induction, rats were randomly divided into two groups which each contained 15 animals: the normal control group (not induced CMS) and the CMS group (negative control). Furthermore, the animal model was performed perfusion to maintain organ when evacuation was done, cell damage did not occur. To evaluate cell organ, immunohistochemistry examination and ELISA examination was performed. All data are presented as mean ± standard deviation and all statistical analyzes are performed with the SPSS 25 (IBM) program. Result This research showed that CMS animal model has a greater duration of immobility than the normal group and serotonin level in CMS animal models decreased almost threefold compared to the normal group. In addition, there were increased expression of caspase-3 indicates that more neuronal cells suffered from apoptosis. So, in this research, it was clearly stated that in depressive disorder, there were elevation of neuronal cell apoptosis in the prefrontal cortex. Conclusion Neuronal cell apoptosis in the prefrontal cortex plays a role in the pathophysiology of depression through activation of negative feedback on serotonin production.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuronal Cell Death Induces Depressive Disorder in Rats Depression-Like Behaviors Caused by Chronic Stress

Hidayat

Saleh

Parisa

2020

SciPsy

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“…Dopaminergic cell death is essential pathophysiology behind the decreased secretion of the neurotransmitter dopamine. Several studies have shown a role for oxidative stress in the initiation of dopaminergic cell damage and death [6], [7], [8]. Oxidative stress is a condition in which oxidative reactions occur in cells, especially the cell membrane due to the large number of oxidants which are unstable compounds due to a lack of one electron.…”

Section: Introductionmentioning

confidence: 99%

Efficacof Cinnamon Extract (Cinnamomum burmannii) as Supplementation in Lir-psychotic-induced Rats through Oxidative Stress Regulation in Neuronal Cells

Hidayat

Wulandari²,

Marchira

et al. 2021

Open Access Maced J Med Sci

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BACKGROUND: Cinnamon is a plant that is often found in Indonesia and is rich in secondary metabolites such as flavonoids, phenols, tannins, and alkaloids. Flavonoids and phenols are very potential as natural antioxidants to suppress various oxidant activities, including oxidant activity that occurs in the hippocampus, which is the underlying psychotic disorder. AIM: This study was aimed to explore the potential of cinnamon extract (CE) on psychotic symptoms. METHODS: Cinnamon simplicia was obtained from the Research and Testing Center for Traditional Medicine, Tawangmangu, Central Java, Indonesia. The extraction of cinnamon was carried out using the maceration method. The animals were subjected to lir-psychotic induction by intraperitoneal injection with ketamine (30 mg/kg BW) for 5 days. The rats were grouped into six groups; each group contained five animals; normal control group, a lir-psychotic group without treatment, lir-psychotic group with haloperidol, lir-psychotic with CE (25 mg/kg BW, 50 mg/kg BW, and 100 mg/kg BW). Oxidative stress in experimental animals was measured by evaluating malondialdehyde (MDA) expression in the brain tissue using immunohistochemical tests. RESULTS: There were differences in clinical symptoms of psychotic disorder in the animal model between before intervention with CE supplementation and after the intervention. The higher the CE dose administered, the better the improvement in psychotic symptoms seen in the psychotic-induced rats. CE supplementation could reduce MDA expression in the hippocampus. This suggests that there was an optimal significance of cinnamon supplementation in reducing oxidative stress from the hippocampus. CONCLUSION: CE was effective in improving psychotic symptoms in lir-psychotic rats through regulation of oxidative stress in neuronal cells.

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Biomolecular Aspects of Schizophrenia

Cited by 2 publications

References 11 publications

Neuronal Cell Death Induces Depressive Disorder in Rats Depression-Like Behaviors Caused by Chronic Stress

Neuronal Cell Death Induces Depressive Disorder in Rats Depression-Like Behaviors Caused by Chronic Stress

Efficacof Cinnamon Extract (Cinnamomum burmannii) as Supplementation in Lir-psychotic-induced Rats through Oxidative Stress Regulation in Neuronal Cells

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