---

Background & Objective: Tetra Carbon Cholride has been known as reference hepatotoxin because it can cause necrosis, fatty change, cirrhosis and cancer liver. Silymarin has hepatoprotective and anti hepatoxin effect. This study was done to determine the protective effect of Silymarin in acute hepatotoxicity of CCl4 in rats.

Materials & Methods: In this experimental study, we chose 25ml/kg dose of CCl4 (in mineral oil solvent) as an optimum dose. The hepatotoxic effects of intraperiotoneal injection of CCl4 for obtaining parameters of toxicity and therapeutic effects have been examined. According to enzymatic results (increase in ALT and AST) and histopathologic changes (grading the changes in liver including cytoplasmic granularity, cloudy swelling, necrosis and fatty change), the interval between prescribing silymarin and sampling  was determined. Silymarin as a suspension in propylene glycol CMC 2% (3/2 ratio) has been prescribed in 50, 200 and 800mg/kg doses and serum and liver samples were obtained. Negative control group received silymarin vehicle in CCl4 solvent, drug control received 800 mg/kg of silymarin in CCl4 solvent and positive control received silymarin vehicle after injecting CCl4.

Results: The results showed that prescribing 50mg/kg silymarin one hour after injecting CCl4, in addition to inhibiting transaminase activity, prevents progress of liver injury up to 50% of positive control group. Cellular repair and regeneration are also enhanced, So the grade 3necrosis in positive control group is decreased to grade 0.5 in silymarin gourp in 48 hours prescribing silymarin (50mg/kg).

Conclusion: This study showed that up to six hours after injecting CCl4 significantly prevents hepatotoxicity, and cause acceleration in repair of liver injuries.

---

Background and Objective: Until now there is no drug formulated to prevent Neuronal Loss following Brain Stroke. In this study, we compared the effects of the mitoKATP opener, diazoxide, on ultra-structural morphology changes following in cortical neurons following in-vivo ischemic injury. Materials and Methods: In this experimental study, Rats randomly allocated in eight experimental groups including sheme, positive control, 1, 5 and 25 mg/kg/body weight of Glybanclamid groups and 2, 6 and 18 mg/kg body weight of Diazoxide experimental groups, respectively. In animals in each experimental groups, only 2 hours following adminstration of Diazoxide or Glybanclamid ischemia was induced for 15 min by the 4-vessel occlusions surgery followed by 24 hours reperfusion. After tissue prosseccing, ultra-structural changes in neuronal mitochondria and nuclei were studied by electromicroscope. Results: Ultrastructural morphological changes including nuclear pyknosis, swollen mitocondria and cristae damage after iscemia were observed in control and sheme groups. These changes were severe in Glybanclamid experimental groups. Also this changes were depend on dosage of Glybanclamid. Ultrastructural changes were decreased in Diazoxide treatment group (18mg/kg body weight), but in 2 and 6mg/kg/body weight of Diazoxide groups these decreasing of Ultrastructural changes was not observed. Conclusion: This study showed that Diazoxide with dosge of 18mg/kg/body weight has neuro-protective effects on diminishing ischemia-induced structural deterioration of neuronal mitochondria and morphological apoptotic changes in nucleus.

---

Background and Objective: Ischemia-reperfusion invoke cell death in hippocampus. This study was carried out to investigate the effect of transforming growth factor alpha (TGF-alpha) of dentyte jyrus neurons and pyramidal cells of CA1 subfiled of hippocampus following ischemia-reperfusion in rat models. Materials and Methods: This experimental study was done on 40 male Wistar rats weighing 250-300gr. Animals were divided in four groups: control (n=7), sham (n=7), ischemia (n=14) and treatment (n=14). Sham group was just under surgical stress. In ischemia and treatment groups after induction of ischemia-reperfiusion by obstruction of carotid arteries blocked for 30 minutes, reperfusion PBS (phosphate buffer salin) and subsequently TGF-alpha (50 ng) were injected stereotaxicaly in lateral ventricle, respectively. In 12 and 72 days after treatment the brains were fixated by transcardial perfusion and stained by immunohistochemestry and nissle methods. Furthermore, morris water maze was used to evaluate the learning memory. Data were analyzed using SPSS-16 and ANOVA test. Results: Injection of TGF-alpha increased the cell number in hippocampus of treatment group compared to ischemic group. TGF-alpha increased expression of neuron in dentyte jyrus of treatment group in comparison with ischemic group (P<0.05). Also spatial memory improved in treatment group in comparison with ischemia group. Conclusion: TGF-alpha improves ischemia-induced neurodegenration and memory impairment.

---

Background and Objective: Reduction in cerebral blood flow following cereblal ischemia cause the production of oxygen free radicals and finally leads to brain tissue destruction. Pyramidal cells of the CA1 region of hippocampus are highly sensitive to hypoxic condition. This study was done to determine the effect of human chorionic gonadotropin (hCG) and vitamine E on cellular density of CA1 hippocampal area, learning ability and memory, following ischemia - reperfusion injury in mice. Materials and Methods: This experimental study was done on 40 male mice in 5 groups as follow: sham control, ischemia, hCG treated, vitamine E treated and hCG + vitamine E treated groups. Single dose of vitamin E was injected intraperitonaly during the establishment of reperfusion and hCG was injected from 48h after ischemia for 5 days. Folowing the treatment period, mice brains were fixated by transcardial perfusion and stained by nissle method. The shuttle box was used to evaluate the learning memory. Results: Co-administartion of vitamine E and hCG, significantly increased the cell numbers in hippocampus compared to the ischemic group (P<0.001). Also learning and memory improved in treatment group in comparison with ischemia group (P<0.05). Conclusion: Co-administration of vitamin E and hCG improved ischemia-induced neurodegenration and memory impairment.