nazem ghasemi

Following exposure to toxic agents, structural and functional changes occur in neurons. These changes can lead to the nervous system dysfunction, such as sensorimotor disorders. In the current study, we investigated how exposure to perfluorooctanoic acid during pregnancy affects the expression of brain-derived neurotrophic factors in the brains of newborn rats.

The brains of newborn Wistar rats which divided into five groups include control, sham and three PFOA receiving groups were used. In the PFOA groups, this compound was gavage with a dose of 1, 5 and 10 mg daily. The brains of newborn mice were removed 20 days after birth and the level of neurotrophic factors derived from these samples was evaluated using ELISA and Real Time PCR methods.

The results showed that the mean expression of the BDNF gene significantly increased in the PFOA-receiving groups compared to other groups (P ≤ 0.001). Also, there was a significant increase in BDNF protein expression in the groups that received doses of 5 and 10 mg of PFOA compared to the control and sham groups (P ≤ 0.05).

The results of this study showed that exposure to a natural pollutant such as PFOA can lead to an increase in BDNF expression, and this increase is probably due to the prevention of the destructive effects of PFOA on the development of the nervous system. Therefore, it is recommended to minimize exposure to PFOA-containing sources as much as possible during pregnancy.

Impairment of the gene expression and nerve growth factors due to exposure to persistent pollutants in nature can lead to functional disorders in the nervous system. In the present study, the effects of exposure to perfluorooctanoic acid (PFOA) on the expression of nerve growth factors in the rat brain were investigated during pregnancy.

The brains of 35 pregnant rats were used. the rats were divided into five groups include: control, sham, 1 mg/kg PFOA group, 5 mg/kg PFOA group, and 10 mg/kg PFOA group. In the group that received PFOA, this compound was gavaged daily. The brains of the newborn mice were removed 20 days after delivery, and the expression of nerve growth factors was analyzed using ELISA and Real-Time PCR methods.

The results showed that NGF gene expression was significantly higher in the PFOA-treated groups, especially in the PFOA/5mg group (P ≤ 0.001). Also, there was a significant increase in NGF protein expression in the 5 mg PFOA dose group (P ≤ 0.01) and the 10 mg PFOA group (P ≤ 0.05) compared to the control and sham groups.

The results of this study showed that exposure to PFOA during pregnancy can lead to increased expression of nerve growth factor. This can prevent the occurrence of neurological disorders caused by exposure to toxic agents.

Previous studies have shown perfluorooctanoic acid (PFOA) causes organ cytotoxicity. There are high levels of PFOA in cord blood that may affect organogenesis. In the present study, the effects of exposure to perfluorooctanoic acid (PFOA) during pregnancy were investigated on the expression of neurotrophin 3 (NT3) and neurotrophin 4 (NT4) factors in the rat brain.

In this study, the newborns brains of 35 pregnant Wistar rats were used. Wistar rats were randomly divided into five groups, including control groups, sham groups, and three groups receiving PFOA at the rate of 1, 5, and 10 mg per kilogram of body weight, were used. In the group receiving PFOA, this compound was given daily using the gavage technique. Using ELISA and Real-Time PCR methods, we investigated the expression of NT3 and NT4 factors in the brain of newborn mice 20 days after birth.

The results showed that the average expression of NT3 and NT4 genes and proteins in the PFOA receiving groups, especially in the 5 and 10 mg PFOA groups, significantly increased compared to other groups (P ≤ 0.001).

The results of the present study showed that exposure to PFOA during pregnancy can lead to increased expression of NT3 and NT4 factors. Increasing these factors by suppressing the oxidant and apoptotic effects of PFOA can prevent PFOA-induced neurological disorders.

Oligodendrocyte apoptosis is one of the principal mechanisms in progressive myelin destruction and the development of neurological disabilities. The oligodendrocyte cell death is usually caused by local inflammation and the toxic effects of some environmental factors. Valproic acid can increase cell survival and differentiation due to its diverse antioxidant, anti-apoptotic, anti-inflammatory, and neuroprotective effects. In the present study, the effects of this compound were investigated in preventing oligodendrocyte cell death in the mouse brain corpus callosum.

In this study, 40 mice were randomly divided into four groups: control, sham, cuprizone, and valproic acid/cuprizone. To kill oligodendrocyte cells, 0.2% caprizone compound was used. In addition, the combination of valproic acid was used intraperitoneally, daily with a dose of 300 mg/kg, and for three weeks. immunohistochemical and real-time methods were used to investigate the specific markers of oligodendrocyte cells.

The results showed that the percentage of cells expressing Oligodendrocyte transcription factor (Olig2) and Myelin oligodendrocyte glycoprotein (Mog) markers increased significantly in the group that received valproic acid compared to the groups that received cuprisone (P < 0.05). Also, an increase in the expression of oligodendrocytes-specific genes was reported in the Real Time-PCR method.

The results of this study showed that valproic acid can prevent oligodendrocyte cell death, therefore, the use of this compound can be a suitable solution to prevent the destruction of myelin in nerve tissue

Environmental toxic factors, with their destructive effects on nerve cells and myelin tissue, can induce nervous system dysfunction. The neuroprotective role of valproic acid as an inhibitor of Glycogen synthase kinase 3β (GSK3-β) has been proven in some neurodegenerative diseases. In the present study, the effects of this combination were investigated in preventing myelin tissue destruction and maintaining its density in the corpus callosum of mouse brain.

40 female C57BL/6 mice weighing 20-25 grams were divided into four groups including control, sham, cuprizone and, valproic acid/cuprizone groups. The valproic acid combination was used intraperitoneally, daily, and at a dose of 300 mg/kg. At the end of the research, to check myelin density, Teloidin blue staining, immunohistochemistry and, real-time methods were used.

The results showed that the density of myelin and the percentage of cells expressing the Myelin Basic Protein (MBP) marker increased significantly in the group that received valproic acid compared to the cuprizone group. In addition, the results of myelin-specific gene expression analysis showed that the use of valproic acid can increase the expression of this gene.

The results of the present study showed that valproic acid has the ability to prevent myelin tissue destruction and maintain its density, and therefore, the use of this combination can be a suitable combination to prevent and reduce the progression of diseases that destroy nerve tissue.

Multiple sclerosis (MS) is the most prevalent neurological disability among young adults. Anti-inflammatory drugs have shown to be effective in MS. The anti-inflammatory and antioxidative properties of Zingiber officinale (ginger) have been shown and proven in many phytotherapy studies. This study aimed to evaluate effects of ginger essential oil on preventing myelin degradation in a rat model of MS. In this study, we divided 49 rats into 7 groups; 4 control and 3 experimental groups that received 3 different dose of ginger essential oil (50, 100, and 150 mg/kg/day) for treatment of cuprizone-induced demyelinated rats. Basket test and transmission electron microscopy were performed in this study. Olig2 and Mbp genes and proteins were respectively evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Histologically, cuprizone created demyelination in the corpus callosum fibers. Remyelination of fibers was seen in the group treated with the medium dose of ginger essence, by toluidine blue staining. transmission electron microscopy (TEM) revealed increased thickness of the myelin of fibers in all 3 treated groups (p<0.05). Feeding by the medium dose of ginger essence significantly increased the levels of Mbp and Olig2 genes (p<0.05).  ELISA test showed that 100 mg/kg/day of ginger caused a significant difference between experimental and the cuprizone-induced groups (p<0.05). Our findings suggested that administration of ginger essential oil prevented demyelination and improved remyelination of rats` corpus callusom and can be used as an effective substance in the prevention of MS.

Many environmental factors are involved in the death of oligodendrocyte cells, myelin tissue destruction, and disturbance in the central nervous system function. The protective role of lithium chloride as a Glycogen synthase kinase 3β (GSK3-β) inhibitor has been proven in some neurological diseases. In the present study, the effects of this compound were investigated in the prevention of oligodendrocytes death in mouse brains.

In the present study, 40 female C57BL/6 mice weighing 20-25 grams were randomly divided into four groups: control, sham, cuprizone, and lithium chloride/cuprizone. Lithium chloride compound was used intra peritoneally daily. At the end of the study, in order to check the results, immunohistochemistry and Real-time PCR were used.

The results of immunohistochemistry staining showed that the percentage of cells that expressed Oligodendrocyte transcription factor (Olig2) and Myelin oligodendrocyte glycoprotein (Mog) markers increased significantly in the group that received lithium compared to the groups that received cuprizone (P < 0.05). In addition, Real-Time PCR results showed that the use of lithium can increase the expression of oligodendrocytes- specific genes.

The results of the present study showed that lithium chloride has the ability to prevent the oligodendrocytes death, and therefore, the use of this compound can be a suitable solution for preventing and reducing the progression of diseases that destroy central nervous tissue.

The disturbance of the myelination process and myelin tissue destruction leads to central nervous system dysfunction. The neuroprotective role of lithium chloride in the treatment of neurological diseases has been proven. In the present study, the effects of lithium chloride in preventing the destruction of myelin tissue induced by cuprizone in the corpus callosum of the mouse brain were investigated.

In this study, 40 female C57BL/6 mice weighing 20-25 grams were randomly divided into four groups including control, sham, cuprizone and lithium chloride/cuprizone groups. The compound of lithium chloride was used intra peritoneally at a dose of 50 mg/kg daily. At the end of the study, in order to check the average myelin density and myelin gene expression, toluidine blue staining, immunohistochemistry and Real Time-PCR were used.

The results of immunohistochemistry and toluidine blue staining showed that, the density of myelin and the percentage of cells which expressing the Myelin Basic Protein (MBP) marker increased significantly in the group which receiving lithium compared to the cuprizone group. In addition, Real Time-PCR results showed that the use of lithium can increase myelin gene expression.

The results of the present study showed that neuroprotective factors, such as lithium chloride, have the ability to prevent the destruction of myelin tissue, and therefore, the use of this combination can be a suitable manner to prevent and reduce the progression of neurodegenerative diseases.

Multiple sclerosis (MS) is known as a nerve tissue disorder, which causes demyelination of central nervous system (CNS) fibers. Cell-based treatment is a novel strategy for the treatment of demyelinating diseases such as MS. Adipose-derived stem cells (ADSCs) have neuroprotective and neuroregenerative effects and pregnenolone as a neurosteroid has remarkable roles in neurogenesis. We intend to examine the impact of intraventricular transplantation of human ADSCs and systemic injection of pregnenolone on the remyelination of a rat model cuprizone-induced demyelination.

This experimental study was performed on 36 male Wistar rats that received a regular diet and a cuprizone diet for 3 weeks for M.S. induction. Through lipoaspirate surgery, human-ADSCs (hADSCs) were obtained from a patient. Six groups of rats (n=6): healthy, MS, sham, pregnenolone injection, ADSCs transplantation, and pregnenolone injection/ADSCs transplantation were included in this study. For assessment of remyelination, transmission electron microscopy (TEM), immunohistochemistry staining, real-time reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay (ELISA) were performed.

TEM outcomes revealed an increase in the thickness of the fibers myelin in the treatment groups (P<0.05). We also observed a significant upregulation of MBP, PDGFR-α, and MOG after treatment with hADSCs and pregnenolone compared to other study groups (P<0.001). These results were confirmed by immunostaining analysis. Moreover, there was no significant difference between the ADSCs/pregnenolone group and the control group regarding the level of MBP, A2B5, and MOG proteins in ELISA.

Our data implied that the remyelination and cell recovery were more improved by intraventricular ADSCs transplantation and pregnenolone injection after inducing a rat model of MS.

Multiple sclerosis (MS) is the most prevalent neurological disability of young adults. Anti-inflammatory drugs have relative effects on MS. The anti-inflammatory and antioxidative effects of Zingiber officinale (ginger) have been proven in some experimental and clinical investigations. The aim of this study was to evaluate the effects of ginger extract on preventing myelin degradation in a rat model of MS.

Forty nine male Wistar rats were used in this study and divided into four control groups: the normal group, cuprizone-induced group, sham group (cuprizone [CPZ] + sodium carboxymethyl cellulose [NaCMC]), standard control group (fingolimod + cuprizone), including three experimental groups of CPZ, each receiving three different doses of ginger extract: 150, 300, and 600mg/kg /kg/day.

Ginger extract of 600 mg/kg prevented corpus callosum from demyelination; however, a significant difference was observed in the fingolimod group (p < 0.05). Difference in the CPZ group was quite significant (p < 0.05).

Treatment with ginger inhibited demyelination and alleviated remyelination of corpus callosum in rats. Therefore, it could serve as a therapeutic agent in the MS.

Growth factors and chemical stimulants have key role in cartilage tissue engineering, but these agents have unfavorable effects on cells. Avocado soybean unsaponifiables (ASU) has chondroprotective and anti‑inflammatory effects. In this study, fibrin2nanoparticles (FNP)/ASU, as a new delivery system, with stem cells applied for cartilage tissue engineering in poly (lactic‑co‑glycolic) acid (PLGA) scaffold.

FNP/ASU prepared by freeze milling and freeze drying. NFP/ASU was characterized by dynamic light scattering (DLS). PLGA‑NFP/ASU scaffold was fabricated and assessed by scanning electron microscope (SEM). Human adipose‑derived stem cells (hADSCs) were seeded on scaffold and induced for chondrogenesis. After 14 days, cell viability and gene/protein expression evaluated.

The results of DLS and SEM indicated that nanoparticles had high quality. The expression of type II collagen and SOX9 and aggrecan (ACAN) genes in differentiated cells in the presence of ASU was significantly increased compared with the control group (P and lt; 0.01), on the other hand, type I collagen expression was significantly decreased and western blot confirmed it.

This study indicated FNP/ASU loaded in PLGA scaffold has excellent effect on chondrogenic differentiation of hADSCs and tissue engineering.

Disruption of myelination process due to exposure to perfluorooctanoic acid (PFOA) can lead to movement disorders. In the present study, the effects of exposure to PFOA during pregnancy on myelin degradation in brain of newborn rat were investigated.

Fertile Wistar rats were randomly divided into five groups of control, sham, and three groups receiving PFOA at doses of 1, 5, and 10 mg/kg body weight. At the end of the study, the brains of 20-day-old neonatal rats were removed and examined using loxal fast blue and immunohistochemical staining. Finally, the data were analyzed using SPSS software. </em>

The mean myelin density in the group receiving PFOA at a dose of 10 mg/kg was significantly lower than the other groups (P < 0.050).

The results showed that exposure to PFOA during pregnancy can lead to disruption of myelin production process; so, it is recommended to avoid exposure to toxic agents such as PFOA during pregnancy.

The progressive destruction of nerve cells in nervous system will induce neurodegenerative diseases. Recently, cell‑based therapies have attracted the attention of researchers in the treatment of these abnormal conditions. Thus, the aim of this study was to provide a simple and efficient way to differentiate human dental pulp stem cells into neural cell‑like to achieve a homogeneous population of these cells for transplantation in neurodegenerative diseases.

In this basic research, human dental pulp stem cells were isolated and characterized by immunocytochemistry and flow cytometry techniques. In the following, the cells were cultured using hanging drop as three‑dimensional (3D) and tissue culture plate as 2D techniques. Subsequently, cultured cells were differentiated into neuron cell‑like in the presence of FGF and Sonic hedgehog (SHH) factors. Finally, the percentage of cells expressing Neu N and β tubulin III markers was determined using immunocytochemistry technique. Finally, all data were analyzed using the SPSS software.

Flow cytometry and immunocytochemistry results indicated that human dental pulp‑derived stem cells were CD90, CD106‑positive, but were negative for CD34, CD45 markers (P ≤ 0.001). In addition, the mean percentage of β tubulin positive cells in different groups did not differ significantly from each other (P ≥ 0.05). Nevertheless, the mean percentage of Neu N‑positive cells was significantly higher in differentiated cells with embryoid bodies’ source, especially in the presence of SHH than other groups (P ≤ 0.05).

It is concluded that due to the wide range of SHH functions and the facilitation of intercellular connections in the hanging droop method, it is recommended that the use of hanging drop method and SHH factor can be effective in increasing the efficiency of cell differentiation.

During pregnancy, the exposure to perfluorooctanoic acid (PFOA) can accompany with oligodendrocyte death. In current study, the effect of exposure to PFOA during pregnancy on the expression of oligodendrocyte markers was investigated.

After Wistar rats’ fertilization, the rats were randomly divided into five groups of control, sham, and three other groups, which received PFOA as 1, 5, and 10 mg/kg body weight. 20-day-old rats were sacrificed, and brain samples were examined using immunohistochemical staining. Finally, the data were analyzed using SPSS software.

In the groups receiving PFOA at doses of 5 and 10 mg/kg, the percentage of Olig2- and myelin-basicprotein (MBP)-positive cells significantly reduced compared to the other groups (P < 0.001).

The findings of this study showed that exposure to PFOA during pregnancy can induce oligodendrocyte death; so it is recommended to avoid exposure to toxic agents such as PFOA during pregnancy.

Multiple Sclerosis is a myelin destroyer disease, which physical activity can be effective in improving it. Therefore, in the present study, the effect of swimming on oligodendrocytic cells and myelin tissue in rat brain of the Cuprizone model of MS disease is investigated.

In this study, 21 male Wistar rats were randomly divided into Control groups, Cuprizone and Swim + Cuprizone. For the induction of MS, Cuprizone 0.6% were gavaged for one month. The group of Swim + Cuprizone swam at the same time with gavage. The training program included 4 weeks of swimming for 5 sessions per week and 30 minutes. Immunohistochemistry technique was used to determine the percentage of immature and mature oligodendrocytes and Luxol fast blue solution for evaluation of myelin density. Image j software and One-way ANOVA was used to analyze the findings.

The mean percentage of immature and mature oligodendrocytes and myelin density in the Swim+Cuprizone group was significantly higher than that of the Cuprizone group (p≤0.05).

Swimming decreases destruction of the oligodendrocytes and myelin cells due to Cuprizone.

Astaxanthin (AST) is a carotenoid with anti-oxidative, anti-inflammatory, and anti-apoptotic properties. It has also been reported that AST exerts protective effects against neurodegenerative diseases and reduces oxidative stress-induced the central nervous system (CNS) injury. In this study, we aimed to evaluate the protective potential of AST in inhibiting demyelination and oligodendrocyte death in a rat model of multiple sclerosis (MS).

In this experimental study, forty Wistar rats were randomly assigned to four experimental groups: control group (with normal feeding), cuprizone (CPZ group) that daily received 0.6% CPZ for 4 weeks, sham group that daily received 0.6% CPZ plus dimethyl sulfoxid (DMSO) for 4 weeks, and AST group that daily received 0.6% CPZ and after 12 hours were treated with AST (3 mg/kg), for 4 weeks. Muscle strength was evaluated by the behavioral basket test at the end of every week for 4 weeks. Luxol Fast Blue (LFB) staining was utilized for the identification of myelination and demyelination. Myelin density was evaluated by the ImageJ software. The expression of A2B5 (oligodendrocyte precursor protein) and myelin oligodendrocyte protein (MOG) were assessed by immunohistochemistry (IHC) and the expression of myelin basic protein (MBP), MOG, and platelet-derived growth factor-alpha (PDGFR-α) genes was examined by the real-time polymerase chain reaction (RT-PCR) technique.

The administration of AST reduced the oligodendrocyte damage and myelin sheath disruption in a rat model of MS. The basket behavioral test showed the improvement of muscle strength in the AST group compared with CPZ and sham groups. Besides, the results of real-time PCR and IHC indicated the beneficial effects of AST in declining demyelination and oligodendrocyte death in a rat model of MS.

AST reduces damages to the myelin sheath and oligodendrocyte death in a rat model of MS.

Nowadays, cartilage tissue engineering is the best candidate for regeneration of cartilage defects. This study evaluates the effect of fibrin/icariin (ICA) nanoparticles (F/I NPs) on chondrogenesis of stem cells.

F/I NPs were characterized by Dynamic Light Scattering DLS. Poly (lactic-co-glycolic) acid (PLGA)-F/I NP scaffold was fabricated and assessed by scanning electron microscope. Human adipose-derived stem cells (hADSCs) were seeded on scaffold and induced for chondrogenesis. After 14 days, cell viability and gene expression were analyzed by the 3-(4, 5- dimethylthiazol-2yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. MTT assay and real-time polymerase chain reaction (RT-PCR).

The size and surface charge of F/I NP were about 28–30 nm and − 17, respectively. The average of pore size of PLGA and PLGA–fibrin/ICA was 230 and 340 μm, respectively. Cell viability of differentiated cells in P/F group was higher than others significantly (P ≤ 0.05). Furthermore, quantitative RT-PCR analysis demonstrated that ICA upregulated cartilaginous-specific gene expression. Furthermore, the results of the expression of type I collagen revealed that ICA downregulated this gene significantly (P < 0.01).

The results indicated that F/I NP could be a potential factor for chondrogenesis of stem cells and downregulation of fibrocartilage marker.

The use of stem cells, growth factors, and scaffolds to repair damaged tissues is a new idea in tissue engineering. The aim of the present study is the investigation of Avocado/soybean (A/S) effects on chondrogenic differentiation of human adipose‑derived stem cells (hADSCs) in micromass culture to access cartilage tissue with high quality.

In this an experimental study After hADSCs characterization, chondrogenic differentiation was induced using transforming growth factor beta 1 (TGF‑β1) (10 ng/ml) and different concentrations (5, 10, and 20 μg/ml) of A/S in micromass culture. The efficiency of A/S on specific gene expression (types I, II, and X collagens, SOX9, and aggrecan) was evaluated using quantitative polymerase chain reaction. In addition, histological study was done using hematoxylin and eosin and toluidine blue staining all data were analyzed using one‑way analysis of variance (ANOVA) and P ≤ 0.05 was considered to be statistically significant.

The results of this study indicated that A/S can promote chondrogenic differentiation in a dose‑dependent manner. In particular, 5 ng/ml A/S showed the highest expression of type II collagen, SOX9, and aggrecan which are effective and important markers in chondrogenic differentiation. In addition, the expression of types I and X collagens which are hypertrophic and fibrous factors in chondrogenesis is lower in present of 5 ng/ml A/S compared with TGF‑β1 group (P ≤ 0.05). Moreover, the sulfated glycosaminoglycans in the extracellular matrix and the presence of chondrocytes within lacuna were more prominent in 5 ng/ml A/S group than other groups.

It can be concluded that A/S similar to TGF‑β1 is able to facilitate the chondrogenic differentiation of hADSCs and do not have adverse effects of TGF‑β1. Thus, TGF‑β1 can be replaced by A/S in the field of tissue engineering.

Multiple sclerosis (MS) is a demyelinating disease that causes chronic inflammation in the central nervous system. The aim of this study was to investigate the effects of apamin administration on myelination process. MS was induced by feeding cuprizone pellets (0.2%) for 6 weeks (demyelination phase) followed by normal feeding for additional 2 weeks (remyelination phase). Briefly, C57BL/6 male mice were randomly divided into six groups. Group 1, received the regular food pellets. Group 2 contained two subgroups of 6 animals each (n = 2 × 6). First group received cuprizone for 6 weeks and the sacrificed while the second group after 6 weeks of cuprizone, received no treatment for additional 2 weeks. Group 3 (co-treatment group) was composed of two subgroups of 6 animals each (n = 2 × 6). Both subgroups received apamin (100 μg/kg) intraperitoneally twice a week for 6 weeks. First subgroup terminated at this time and the second subgroup was fed normal diet for two additional weeks. Group 4 (post-treatment, n = 6) received apamin (100 μg/kg) intraperitoneally twice a week for 2 weeks after cuprizone secession. Groups 5 and 6 (vehicle, n = 6 in each group) received phosphate buffered saline as the vehicle of apamin during demyelination and remyelination phase. At the end of each phase, mice were deeply anesthetized and perfused. Groups 5 and 6 (vehicle) received PBS as the vehicle during both phases. Mice were anesthetized, perfused with PBS through their heart, and their brains were removed. Brain sections stained with luxol fast blue and the images were analyzed. Apamin co-treatment significantly increased the myelin content as compared to the cuprizone group. Also, mild elevation in the myelinated areas was observed with apamin post-treatment in comparison with remyelination phase. Our results revealed that apamin prevents myelin destruction more significantly as compared to remyelination process. This observation explains the possible role of apamin in inhibiting   the activation of the microglia cells than stimulation of the oligodendrocytic precursor cells.

The striatal dopamine (DA) deficiency is known as the main cause of the clinical picture of Parkinson’s disease (PD). The disease is a progressive degeneration of dopaminergic neurons in the striatum. The treatment of PD is based on compensation for the brain's supply of DA lost by drug therapy, deep brain stimulation, surgery, gene and cell therapies. Clinical studies have focused on the utility of stem cell-based therapies in PD. Embryonic and mesenchymal stem cells (MSCs) are widely used. Recently, human adipose derived stem cells (hADSCs) have been considered as a suitable source of tissue for this purpose. In this project, hADSCs differentiated into dopaminergic neurons and the specificity of the cell preparations was examined. Human adipose tissues were collected from healthy volunteers undergoing liposuction and hADSCs were isolated by collagenase-based enzymatic method. Flow cytometry was performed using the surface cluster of differentiation (CD) markers to confirm the cell typical properties. Then hADSCs were differentiated to dopaminergic neurons in neurobasal medium in the presence of differentiation factors and confirmed by immunocytochemistry via neuronal and dopaminergic markers. The isolated hADSCs were cultured and identified by the expression of MSCs surface markers including CD90, and CD44.These cells did not express hematopoietic surface markers such as CD45 and CD14. Differentiated cells express neuronal marker NeuN and dopaminergic marker tyrosine hydroxylase (TH). It is concluded that hADSCs can be easily taken from the patient's own body and differentiated into dopaminergic cells having a lower risk of transplant rejection.

Multiple sclerosis (MS) is a chronic and multiphasic autoimmune disease which affecting the nervous system. Recently, neurotrophic factor secreting cells have been proposed as one of the best sources for cell therapy in MS disease. Therefore, this review study was done with aimed to introduce neurotrophic factor secreting cells and the role of neurotrophic factors in the treatment of MS. The present study, based on the Systematic Review and using multiple sclerosis, neurotrophin and cell therapy keywords, 98 articles were searched from various databases including Pubmed, SID, Springer, SinceDirect Magiran, Web of Sciences and the Google Scholar. After removing irrelevant and repetitive articles, 50 articles were selected. The results of these studies showed that cell-based therapies in MS have been designed with the aim of replacing destroyed cells or with the goal of neuronal support using neural growth factors. Neurotrophic factors secreting cells with the ability to migrate to neurological lesions and secretion of neurotrophic factors can play a major role in supporting neural tissue and preventing its destruction. These factors, through tyrosine kinase receptors, have a variety of effects on the development and proper functioning of neurons. On conclusion, neurotrophic factor secreting cells due to the secretion of a wide range of neural growth factors which required for neural development might be one of the ideal cell sources for cell-based therapy in MS disease.

Multiple sclerosis is a chronic neurodegenerative disease which is accompanied by neurological disability. Curcumin can be effective in prevention of this abnormal condition because of its ability to cross the blood-brain barrier, its potent antioxidant effect and nerve protective effects. The aim of this study was to evaluate curcumin effects on improvement of muscle strength, prevention of degradation of oligodendrocytes cells and myelin in rat brain. Twenty eight rats (wt:200 g) were randomly divided into four groups: control, sham (DMSO), cuprizone and curcumin. Curcumin group, received cuprizone (0.6%) gavage and curcumin (200 mg / kg) simultaneously for four weeks. During the study we evaluated muscle strength by using a behavioral basket test, the percentage of cells expressing A2B5 and MBP markers by immunohistochemistry technique. Myelin density was evaluated by luxol fast blue staining. Using Image J and SPSS softwares, the results were analyzed by one-way ANOVA test. Immunohistochemistry images showed that the percentages of mature oligodendrocytes and oligodendrocytes progenitor cells in the curcumin group were significantly higher than those in the sham and cuprizone groups (p≤0.05). In addition, myelin density and muscle strength were higher in the curcumin group compared to those in the cuprizone and sham groups (p≤0.05). The consumption of natural compounds containing curcumin, can be effective in the prevention of oligodendrocytes and myelin destruction in people susceptible to MS

Learning skull radiography techniques is time consuming and difficult, due to the variety of these techniques. Each year, poor employee performance of the radiology unit, impose repetitive radiographs, and a heavy burden on the health system, as well as double exposure of patients and staff. According to the results of the current investigation, comparing student’s opinions revealed that the use of flash cards could facilitate and accelerate learning of radiographic techniques. Moreover, it is demonstrated that using flash cards could help maintain long-term radiographic techniques and are effective in the education process. This report highlights that the use of flash cards not only facilitates and accelerates the learning of the skull radiographic techniques, but also can reduce the repetitive radiographs, the costs imposed on the health system and double exposure of patients and staff.

Multiple Sclerosis (MS) has been explained as an autoimmune mediated disorder in central nerve system. Since conventional therapies for MS are not able to stop or reverse the destruction of nerve tissue, stem cell-based therapy has been proposed for the treatment of MS. Astaxanthin (AST) is a red fat-soluble xanthophyll with neuroprotection activity. The aim of this study was evaluation of pre-inducer function of AST on differentiation of human Adipose- Derived Stem Cells (hADSCs) into oligodendrocyte precursor cells.
After stem cell isolation, culture and characterization by flow cytometry, hanging drop technique was done for embryoid body formation. In the following, hADSCs were differentiated into oligodendrocyte cells in the presence of AST at various concentrations (1, 5, and 10 ng/ml). Finally, immunocytochemistry and real-time PCR techniques were used for assessment of oligodendrocyte differentiation.
Flow cytometry results indicated that hADSCs were CD44, CD49-positive, but were negative for CD14, CD45 markers. In addition, immunocytochemistry results revealed that, in AST treated groups, the mean percentage of Olig 2 and A2B5 positive cells increased especially in 5 ng/ml AST treated group compared to control group (p Since hADSCs have the potential to differentiate into multi lineage cells and due to important functions of AST in regulating various cellular processes, it seems that AST can be used as a promoter for oligodendrocyte differentiation of hADSCs for being used in cell transplantation in multiple sclerosis.

Stem cell-based therapy is a new method for the treatment of neurodegenerative diseases such as multiple sclerosis (MS). Human adipose-derived stem cells (hADSCs) are a kind of adult stem cells which have a higher frequency in the fat tissue and have the ability to differentiate into other cell types outside their lineage. Due to some serious adverse events of cell-based therapy such as tumorigenic potential, the aim of this study was to evaluate of hADSCs differentiation into oligodendrocytes as a valuable way for future cell transplantation.

hADSC were isolated from lipoaspirate samples of human abdominal fat. After hADSC characterization via flow cytometry, the cells were induced to oligodendrocytes using a special differentiation medium. Finally, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), immunocytochemistry, and real-time polymerase chain reaction (RT-PCR) techniques were used for the evaluation of differentiated cells.

Flow cytometry indicated that hADSCs were CD105- and CD49-positive, but were negative for CD31 and CD45 markers. In addition, immunocytochemistry analysis revealed that a high percent of differentiated cells expressed oligodendrocyte progenitor cells markers [A2B5 and oligodendrocyte transcription factor (Olig2)] which were significantly higher than myelin basic protein (MBP) which is mature oligodendrocytes marker. Moreover, a very low percentage of differentiated cells expressed glial fibrillary acidic protein (GFAP) marker. Finally, real-time reverse transcription PCR analysis confirmed the results of immunocytochemistry.

Since hADSCs have the potential to differentiate into multi-lineage cells and due to their additional characteristics such as immunomodulatory and neuroprotective properties, it seems that these cells may be an ideal cell source for oligodendrocytes differentiation.