ABSTRACT
ABSTRACT Objective: To investigate the effects of buserelin on the development of follicles, apoptosis index and steroid hormones level. Methods: Twenty-four 3-month-old female rats were randomly divided into three groups: a low-dose group, a high-dose group and a control group (n = 8). Buserelin and normal saline were injected subcutaneously for 5 days. Thirty days after the first injection, the ovaries were removed for staining. Blood samples were collected and centrifuged. Their serum was used for measuring estradiol and progesterone levels, using enzyme-linked immunosorbent assay. Results: The findings revealed a significant decrease in the mean of secondary and Graafian follicles in the high-dose group compared with the control group (p = 0.037, p = 0.034, respectively). The serum estradiol level increased significantly in the high-dose group, compared with the low-dose and control groups (p = 0.027, p = 0.047, respectively). The serum progesterone level decreased, although not significantly. In contrast to the control group, the significant increase of apoptotic cell death was found in primordial, unilaminar and multi-laminar follicles in the high-dose group (p = 0.004, p = 0.049, p = 0.047, respectively). Conclusion: The findings of this study suggest that short-term administration of high-dose buserelin increases the serum estradiol level and apoptosis in the granulosa cells but has an inhibitory effect on follicular development.
ABSTRACT
Hippocampal neural stem/progenitor cells (hipp-NS/PCs) of the adult mammalian brain are important sources of neuronal and gial cell production. In this study, the main goal is to investigate the plasticity of these cells in neuronal/astroglial differentiations. To this end, the differentiation of the hipp-NS/PCs isolated from 3-month-old Wistar rats was investigated in response to the embryonic cerebrospinal fluid (E-CSF) including E13.5, E17-CSF and the adult cerebrospinal fluid (A-CSF), all extracted from rats. CSF samples were selected based on their effects on cell behavioral parameters. Primary cell culture was performed in the presence of either normal or high levels of KCL in a culture medium. High levels of KCL cause cell depolarization, and thus the activation of quiescent NSCs. Results from immunocytochemistry (ICC) and semi-quantitative RT-PCR (sRT-PCR) techniques showed that in E-CSF-treated groups, neuronal differentiation increased (E17>E13.5). In contrast, A-CSF decreased and increased neuronal and astroglial differentiations, respectively. Cell survivability and/or proliferation (S/P), evaluated by an MTT assay, increased by E13.5 CSF, but decreased by both E17 CSF and A-CSF. Based on the results, it is finally concluded that adult rat hippocampal proliferative cells are not restricted progenitors but rather show high plasticity in neuronal/astroglial differentiation according to the effects of CSF samples. In addition, using high concentrations of KCL in the primary cell culture led to an increase in the number of NSCs, which in turn resulted in the increase in neuronal or astroglial differentiations after CSF treatment.
ABSTRACT
To investigate direct gonadal effect of buserelin as an agonist of gonadotrophin releasing hormone, the incidence of apoptotic cell death was measured. Thirty 25-day-old immature Wistar male rats were divided into two groups: treated and control rats. Treated rats were given 1.25 mg buserelin acetate/g body weight control rats received vehicle subcutaneously for 5 days. Formalin-fixed paraffin embedded testicles were then investigated for the morphology of seminiferous tubules and occurrence of apoptosis using haematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling respectively. Immaturity of rats was proved by the morphological characteristics of testis. In contrast to the control rats, significant increase of apoptotic cell death was found in buserelin-treated rats. Apart from the well-known pituitary-testicular function of buserelin as an agonist of gonadotrophin releasing hormone, our findings suggest that it induces apoptotic cell death via direct gonadal action.
