ABSTRACT
Ovarian and steroid hormones have long and short-term effects of brain. Progesterone has functional and structural effect on Hippocampus neurons. In epilepsyprobably the number of brain neurons can reduce due to cell mortality. Therefore, in this study effect of progesterone were evaluated on the number of CA3 Hippocampus neurons. In this experimental study, 45 Male wistar rats were divided into 5 groups. 5 rats selected as an intact group. Group1 [control] were received, 50-mg/kg- pentylenetetrazd [PTZ]i.p. for kindling. Group 2 received PTZ sesom oil [i.p][vehicle], 30 min before, groups 3 and 4 received 25 and 50 mg/kg progesterone [i.p] 30 min before receiving PTZ. PTZ injected every 48 h and the rate of mortality, seizure stage and duration of V phase were calculated during in min after PTZ injection. If animal reach to phase 5, for three times they were considered as kindled rats and anesthetized by ether for histological study. Their brain were perfuse for fixation by formaldehyde [10%]. and after passage and blocking, 10 micron slices prepared and stained with HandE and Cresyl violet methods. Then CA3 neurons were counted with morphometric lens per mm[2]. The results were shown that injection of 25 and 50mg/kg progesterone reduced duration of phase V from 175.2 S in sham to 123.1 S and 113.1 S respectively, [p<0.05 and p0.01]. PTZ reduced the number of CA3 neurons form 178.3 +/- 8 in intact animals to 123.2 +/- 14.2 in control [p<0.05]. The mean number of neurons in 25 and 50 mg/kg progesterone were 137.3 +/- 10.5 and 145 +/- 8.5 respectively. The number of CA3 neuron in 50mg/kg progesterone group had significant difference compared to control group [p<0.05].The results of this study showed that, neuron mortality due to PTZ, reduced in progesterone receiving group compared to control. It seem that there is correlation between neuron mortality and phase 5 duration in progesterone receiving group
ABSTRACT
Since in diabetes the permeability of vessels is impaired, therefore late onset complications of diabetes originated from vascular changes. Calcium plays a major role in inducing and starting process that cause vascular injury and increased permeability. The aim of this study was to indicate whether calcium channel blockers [nifedipine and verapamil] could prevent vascular permeability. In this experimental interventional study, male rats, divided into seven groups randomly. Diabetes induced by subcutaneous injection of 50 mg/kg streptozotocin. Vasculopathy was evaluated by extravasations of Evans blue dye and water content of tissue. Animals received 40 mg/kg of verapamil and 10 mg/kg of nifedipine orally daily. Results of this study showed that extravasations of Evans blue dye was increased significantly [P<0.001] in diabetic group compare to control group, while verapamil decreased extravasations of Evans blue significantly compare to diabetic control group [P<0.01], however nifedipine had no inhibitory effect an water content of tissues did not change significantly. The body weight of animals in diabetic group decreased significantly [p<0.05] at the end of experiment compare to the beginning of experiment, but verapamil and nifedipine have prevented the decrease of body weight in diabetic group. The results of this study suggest that using calcium channel blockers particularly verapamil can inhibit diabetic vasculopathy and prevent the body weight reduction effectively