Journal of Arak University of Medical Sciences

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Showing 3 results for Sanadgol

Study of the Effects of Ellagic Acid on Population and Activity of Central Nervous System Neuroglia Cells in the Cuprizone-induced Multiple Sclerosis

Nima Sanadgol, Parisa Maleki,
Volume 21, Issue 6 (12-2018)

Abstract

Background and Aim: Ellagic acid (EA) is a natural antioxidant with phenolic structure. In this study, we evaluate the effects of EA consumption on population and activation of neuroglia cells in the animal model of MS under oxidative stress.
Materials and Methods: Mature male mice with age of between 8 to 9 weeks were kept in the standard conditions. For model induction, animals received powder normal diet containing 0.2% Cuprizone (Cup) for six weeks. Mice were divided into eight groups containing control, control receiving three doses of EA (20, 40 and 80 mg/kg), Cup and Cup receiving three doses of EA. Finally, specific glial cell markers in the animal brain tissues were analyzed by molecular methods such as immunohistochemistry (IHC), western blotting (WB) and Real Time-PCR (RT-PCR).
Findings: IHC and WB analysis have shown that only high concentration of EA is able to reduce protein expression of GFAP (activated astrocytes marker), Mac-3 (activated microglial marker), increase protein expression of Olig-2 (oligodendrocytes precursor marker) and ultimately significant reduction on APC (mature oligodendrocytes marker)/Olig-2 ratio in comparison with Cup group. In addition, RT-PCR evaluation indicated that changes in the mRNA expression of target markers were consistent with observed changes in their protein expression and therefore, IHC and WB results were confirmed.
Conclusion: Consumption of 80 mg/kg of EA effectively decreased activation of astrocytes and microglial and so appropriates environment for migration of oligodendrocyte precursor cells to the lesion area and shifting from damage course into the repair progressions.

Evaluation of Effects of Benzoaric Acid on the I-KB/NF-Kb Complex and Expression of Caspase-8 and -9 in Animal Model of Multiple Sclerosis

Nima Sanadgol , Mohammad Sharifzadeh , Parisa Maleki ,
Volume 22, Issue 3 (8-2019)

Abstract

Background and Aim: Regarding the importance of new treatments to control and treat multiple sclerosis (MS), in this study we investigated the role of Benzoaric acid (BA) on the neuro-inflammation and apoptosis processes in the cuprizone (cup)-induced animal model of MS.
Materials and Methods: In this experimental study, 35 males C57BL/6 mice were divided into five groups. The study groups were included, control: received six weeks of normal powdered food beside intraperitoneal (i.p.) injection of BA solvent (100 µL per day PBS) for the last two weeks, cup: received six weeks of powdered food contains 0.2% cup beside i.p. injection of BA solvent for the last two weeks and cup-treatment: received six weeks of powdered food contains 0.2% cup beside i.p. injection of 20, 40 and 80 mg/kg BA for the last two weeks. Eventually, the medial corpus callosum area of the animal’s brain was evaluated via western blot and Real-Time PCR methods.
Ethical Considerations: Ethical points were observed according to the declaration of Helsinki and relevant code of ethics, regarding minimizing harms during animal experimentation (UOZ-GR-9517-13).
Findings: Molecular studies have shown that BA-80 decreased mRNA (p <0.01) and protein expression of NF-KB and consequently increased I-KB/NF-KB ratio (p <0.05) and decreased inflammation in compare to cup group. Moreover, BA-80 decreased caspase-9 mRNA (p<0.01) and caspase-8 mRNA (p <0.05) and subsequently increased caspase-8/caspase-9 ratio (p<0.01) and decreased apoptosis in compare to cup group.
Conclusion: The dose of 80 mg/ml BA via decreasing cup-induced neuro-inflammation and neuro-apoptosis has protective effects in this model.

Expression Changes of Genes Involved in Autophagy of the Endoplasmic Reticulum Network in Animal Models of Alzheimer’s Disease

Zakiyeh Gharib, Naser Sanchooli, Nima Sanadgol,
Volume 23, Issue 2 (June & July 2020)

Abstract

Background and Aim: This study aimed to investigate the association between Endoplasmic Reticulum autophagy (ER-phagy) and Alzheimer’s Disease (AD) by analyzing the expression patterns of related genes in animal models.
Methods & Materials: Microarray data of AD patients’ brain tissues were extracted from the Gene Expression Omnibus (GEO) database. These data were first analyzed in GEO2R online tool. Then, the expression of ER-phagy related genes were isolated and the protein interaction networks were plotted by STRING database for the genes with increased expression. Finally, the relationship between the genes that had significant increased expression were designed, and the expression of new identified genes in each study was examined.
Ethical Considerations: All ethical principles were considered in this article.
Results: Genes involved in ER-phagy showed a sporadic expression in different AD models. An increase in the expression of ER-phagy regulatory 1 (FAM134B) gene was observed in studies with the mutation in both Microtubule-associated Protein Tau (MAPT) and Amyloid Precursor Protein (APP) genes. Increase in the expression of NPC intracellular cholesterol transporter 1 (NPC1) gene was observed in two studies that had mutations in APP, Presenilin 1 (PSEN1) and MAPT genes. Moreover, SEC62 homolog and Cell Cycle Progression 1 (CCPG1) genes both showed decreased expression in one study. Finally, the expression of Reticulon 3 (RTN3) was not significant in any of the studies.
Conclusion: The genes involved in ER-phagy have a sporadic expression in AD models, where only two genes FAM134B and NPC1 are involved in AD. The FAM134B gene seems to interact with the Wnk1 gene, which plays a role in cell survival and proliferation, in the hippocampus and forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. NPC1 had interaction with the Abcg1 gene, which activates lipid homeostasis, in the subventricular zone.

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