Experimental Study of Apoptosis after Castration in Prostate Tissue

Abstract: The prostate gland is one of the reproductive enclosure glands that its physiological function is necessary for successful reproduction in males. This gland depends on sexual hormones including androgens for its natural function and normal growth and development. So in the case of hyperplasia, hypertrophy or other prostate diseases, the most successful and efficient method of treatment is castration that in some cases is unavoidable. This thesis has been done to survey the effects of the androgen depletion states on the prostate gland and for determining the mechanism of cell death engaged in this state. In this thesis we used two groups of dogs that each group contained 5 dogs. These dogs were under care for 1 month. In this period of time they were surveyed for any possible disease. After this period the dogs in "treatment group were castrated for decreasing the level of the androgen hormones in the blood. The dogs in the "control group" were left intact. After a week of surgery, prostate glands of these dogs were extracted and used for preparing pathological cross sections. These sections have been colored in the TUNEL and H&E methods and then inspected with optical microscope for detecting apoptotic cells. We found that after castration, the size of the prostate gland decreases and microscopically changes of the gland include increased number of apoptotic cells. These results demonstrate that the type of the cell death engaged in prostate gland in androgen deprivation states are Apoptosis

Osseous reaction to implantation of two endodontic cements : mineral trioxide aggregate (MTA) and calcium enriched mixture (CEM)

Aim: The aim of the present in vivo study was to determine bone tissue reaction to calcium enriched mixture (CEM) and mineral trioxide aggregate (MTA) using a rat femur model. Study Design: Sixty-three rats were selected and randomly divided into three groups of 21 each [experimental groups (n=15), control (n=6)]. Implantation cavities were prepared in each femoral bone and randomly filled with the biomaterials only in the experimental groups. The animals in three groups were sacrificed 1, 4, and 8 weeks postoperatively. Histologic evaluations comprising inflammation severity and new bone formation were blindly made on HE-stained decalcified 6-?m sections. Results: At 1, 4, and 8 weeks after implantation number of inflammatory cells had decreased in the CEM, MTA and control groups, respectively, with no statistically significant differences. Conversely, new bone formation had increased in all the experimental and control groups, without statistically significant differences. Conclusion: The results suggest that biocompatibility of MTA, as gold standard, and CEM cement as a new endodontic biomaterial are comparabl

Protective effects of Crocin on experimental hepatic ischemia-reperfusion injury in the rat

Ischemia followed by reperfusion (I/R) may cause metabolic and structural hepatic damage. The aim of this study was to investigate the effects of crocin on liver ischemia/reperfusion (I/R) injury in rats. For this purpose a total of 40 male Wistar rats were randomized into four groups of ten: (1) controls: including unmanipulated rats; (2) sham group: rats subjected to the surgical procedure, except for liver I/R, and given saline; (3) I/R group: rats underwent liver ischemia for 45 minutes followed by reperfusion for 45 minutes; (4) I-R/Crocin group: rats pretreated with crocin (200 mg/kg, ip). Blood samples and liver tissues were harvested from the rats, and then the rats were sacrificed. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels were determined. Malondialdehyde (MDA) and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were assayed in liver homogenates. Also liver tissue histopathology was evaluated by light microscopy. In group 4, crocin significantly (

Corresponding Author Antinecroinflammatory Effects of Atorvastatin Against Carbon Tetra Chloride-induced Hepatotoxicity in Rats Antinecroinflammatory Effects of Atorvastatin Against Carbon Tetra Chloride-induced Hepatotoxicity in Rats

ABSTRACT Atorvastatin is widely used in the treatment of hepatic disease. The aim of present study is to determine the necroinflammatory activity of atorvastatin against CCl 4 -induced hepatotoxicity in rats. 30 Adult Wistar male albino rats were collected and these rats divided randomly into 5 groups. Group I was as Control group and received intraperitoneal injection of saline (1mg.kg -1 ), Group II received CCl (1 mg/kg, s.c), Group III received Atorvastatin (5 mg/kg, p.o) +CCl (1 mg/kg, i.p), Group IV received Atorvastatin (10 mg/kg, p.o) +CCl (1 mg/kg, i.p) and Group V received Atorvastatin (15 mg/kg, p.o) +CCl (1 mg/kg, i.p) for 28 consecutive day. At the 28 day blood samples from all rats of every group were collected and levels of SGPT, SGOT, ALP and Bilirubin by standard kits were assayed. The liver tissues were taken for histopathological examination. From histopathological study in group I no abnormal changes were observed and in group II, III and IV different abnormal changes with different degrees consist of fatty change, lymphocytic infiltration, necrosis, congestion and hemorrhage were distinguished.in end for Group V no fatty change were observed and was similar to normal hepatocyte. The animals treated with CCl 4 exhibited a significant (P<0.001) rise in SGOT, SGPT, ALP and bilirubin levels when compared to the control group. The results of this study clearly demonstrated that the atorvastatin exhibited potent hepatoprotective activity against CCl 4 -induced hepatic damage in rats. This may be due to their antioxidant and free radical scavenging properties. In this study, an increase in the activities of SGPT, SGOT, ALP and bilirubin in serum evidenced the CCl4 -induced hepatocellular damage because these are cytoplasmic in location and are released into the circulation after cellular damage

Investigating the Protective effect of hesperetin in high fat diet-induced fatty liver disease in rat

Background & Objective: Fatty liver disease as the most common type of liver disease, is usually accompanied with obesity, hyperlipidemia, and diabetes mellitus Type 2. The aim of the present study was to evaluate the protective effects of Hesperetin on high fat diet-induced hepatic steatosis. Material & Methods: Thirty two Wistar male rats were treated in 4 experimental groups including: control group, high fat diet group, high fat diet plus Clofibrate as positive control, and high fat diet plus Hesperetin powder (5 mg/kg), at a period of 6 weeks. At the end of experiment, the groups were compared considering serum lipid profile, serum biomarkers of liver tissue injury and antioxidant activity of liver, using ANOVA test. Histopathology of liver was carried out for confirming the biochemical findings. Results: There were significant changes as shown by the results. In high fat diet group, hypertriglyceridemia, hypercholesterolemia, significant increased activities of hepatocellular enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) in plasma, significant decline in antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase), and elevated lipid peroxidation indices in liver were seen (p<0.01). Hesperetin treatment significantly reduced elevated markers of liver tissue injury and marker of lipid peroxidation (malondialdehyde), and returned the liver antioxidants and the increased serum lipids towards normal (p<0.05). Histopathological examination of liver tissue was consistent with biochemical changes. Conclusion: The results showed that Hesperetin exerts protective effects against hepatic steatosis in rats fed with high fat diet through its antioxidant action

Study on protective effect of Naringenin (Citrus flavonone) on incipient diabetic hepatopathy in alloxan-induced diabetic rats

Abstract    Diabetes mellitus is a metabolic disorder and its incidence is considered to be high all over the world. Hepatic insufficiency is one of the most important consequences in this disease. A multitude of drugs has been described for the treatment of diabetes throughout the world. The aim of the present study was to assess the protective effect of Naringenin on early liver injury in alloxan-induced diabetic rats. Forty male Wistar rats were randomly assigned into 4 different groups of 10 rats each, including healthy control rats, normal healthy rats receiving Naringenin (50 mg/kg), diabetic rats and diabetic rats receiving Naringenin (50 mg/kg). Diabetes was induced with a single injection of alloxan (120 mg/kg i.p.). Naringenin groups received the drug daily for 3 weeks through gavage. At the end of the experiment, levels of liver function marker enzymes AST (Aspartate aminotransferase), ALT (Alanine aminotransferase) and ALP (Alkaline Phosphatase), TB (Total Bilirubin), Alb (Albumin) and TP (Total Proteins) were assessed in serum. Product of lipid peroxidation (Malondialdehyde; MDA), activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GR) were also assayed in liver homogenate to evaluate antioxidant activity. Moreover, histopathological observations were made to assess the degree of hepatic injury. In alloxanized diabetic rats, Naringenin significantly decreased the levels of serum biomarkers of hepatic injury and TB, and elevated the levels of Alb and TP. Furthermore, Naringenin significantly decreased the lipid peroxidation and elevated the levels of antioxidant enzymes in these rats. Histopathological changes were in agreement with biochemical findings. The findings of this study indicated that Naringenin due to its antioxidant activities protects rats liver from early diabetic hepatopathy