nahid rahbar roshandel

In the present study, we investigated the effects of noscapine (0.5-2 µM), an alkaloid from the opium poppy(Papaver somniferum), on primary murine cortical neurons exposed to 60 min oxygen–glucose deprivation (OGD) in the presence of 5 µM BD-1047, a selective sigma-1 receptor antagonist. The experiments were performed on cortical neurons after 11–16 days of culture. To initiate oxygen–glucose deprivation, the culture medium was transferred to glucose-free DMEM, and placed in a humidified incubation chamber containing a mixture of 95% N2 and 5% CO2 at 37 °C for 60 min. In order to explore the effect on neurons under oxygen–glucose deprivation in this condition, some cultures were pretreated with noscapine and BD1047 together, 24 h prior to OGD followed by 24 h recovery. Cell viability, nitric oxide (NO) production and intracellular calcium concentration ([Ca2+]i) levels were evaluated by MTT assay, the modified Griess method, and Fura-2, respectively. Pretreatment of the cultures with noscapine in the presence of BD1047 significantly increased cell viability and decreased NO generation in a dose-dependent manner compared to BD1047 alone. Pretreatment with 2 μM noscapine and BD-1047 was shown to decrease the rise in [Ca2+]i induced by sodium azide (NaN3) and glucose deprivation. We concluded that noscapine in the presence of BD1047 could protect primary cortical neurons after oxygen–glucose deprivation-induced cell injury but this effect was not complete. Our results indicate that neuroprotective effects of noscapine could be mediated partially through activation of sigma-1 receptor and by decreasing NO production and [Ca2+]i levels.

Alzheimer’s disease (AD) is characterized by progressive neuronal loss in hippocamp. Epidermal neural crest stem cells (EPI-NCSC) can differentiate into neurons, astrocytes and oligodendrocytes. The purpose of this study was to evaluate the effects of transplanting EPI-NCSC into AD rat model. Two weeks after induction of AD by injection of Amyloid-β 1-40 into CA1 area of rat hippocamp, Y-maze and single-trial passive avoidance tests were used to show deficit of learning and memory abilities. EPI-NCSC were obtained from the vibrissa hair follicle of rat, cultured and labeled with bromodeoxyuridine. When Alzheimer was proved by behavioral tests, EPI-NCSC was transplanted into CA3 area of hippocamp in AD rat model. The staining of EPI-NCSC markers (nestin and SOX10) was done in vitro. Double-labeling immunofluorescence was performed to study survival and differentiation of the grafted cells. We showed that transplanted EPI-NCSC survive and produce many neurons and a few glial cells, presenting glial fibrillary acidic protein. Total number of granule cells in hippocamp was estimated to be more in the AD rat model with transplanted cells as compared to AD control group. We observed that rats with hippocampal damage made more errors than control rats on the Y-maze, when reward locations were reversed. Transplanted cells were migrated to all areas of hippocamp and the total number of granule cell in treatment group was equal compared to control group. Transplantation of EPI-NCSC into hippocamp might differentiate into cholinergic neurons and could cure impairment of memory in AD rat model.

Transplants of multipotent stem cells have been shown to have a neuroprotective effect after central nervous system injury. The bulge region of the hair follicle has been reported as a putative source of hair follicle stem cells (HFSC) for many years; however, few studies have documented the properties of bulge derived cells in vitro until now. This study was conducted to isolate and culture bulge cells from rat hair follicles and to determine the morphological and biological features of the cultured cells. The bulge region of the rat whisker was isolated and cultured in Dulbecco's modified eagle medium: nutrient mixture F-12 (DMEM/F12) supplemented with epidermal growth factor (EGF), cholera toxin. Dissociated bulge stem cells were differentiated on coated substrates together with NT-3. The morphological and biological features of cultured bulge cells were observed by light microscopy and immunocytochemistry methods. Our results showed that newly proliferated cells could be observed on the 4th day after explantation. The expression of a neural progenitor marker, nestin, was seen before differentiation of the bulge cells. The differentiated cells expressed βIII-Tubulin and RIP, which are the markers of neural and glial lineages. The results indicated that the bulge cells cultured from the rat hair follicle had the characteristics of stem cells and could differentiate into neural and glial lineages.

The protective effect of a L-type calcium channel blocker, nimodipine, on cell injury induced by oxygen-glucose deprivation (OGD) in PC12 cells was investigated. PC12 cells were exposed to in-vitro oxygen-glucose deprivation (30 minutes and 60 minutes respectively) in the presence or absence of nimodipine (10mM/L) in three different time schedules (pre-24h, pre-3h and concurrently). Cellular viability was assessed by MTT assay. OGD-induced cell injury was significantly attenuated by nimodipine in all three treatment schedules. Application of MK801 (10mM/L), an antagonist of NMDA glutamate receptors also inhibited PC12 cell death by OGD method. Our study suggests that nimodipine has protective effects against OGD-induced neurotoxicity.