The ultrastructural alterations in rat corneas with experimentally-induced diabetes mellitus

Objectives: To examine the ultrastructural changes of rat comeas in streptozotocin (STZ) induced diabetes mellitus and the follow-up insulin treatment

Effect of fluoride intoxication on endometrial apoptosis and lipid peroxidation in rats: Role of vitamins E and C

Fluoride is a strong, hard anion and cumulative toxic agent. The effect of fluoride intoxication on lipid peroxidation in endometrial tissue and the protective effects of combinations of vitamins E and C in rats were studied. Additionally, the apoptotic changes in er dometrial tissue were examined. Experimental groups were as follows: control group; a group treated with 100 mg/l fluoride (F group); and a group treated with 100 mg/l fluoride plus vitamins E and C (F + Vit group). The F and F + Vit groups were treated orally with fluoride for 30 days. Vitamins E and C were injected simultaneously at doses of 50 mg/kg day i.m. and 20 mg/kg day body weight i.p. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick and labeling (TUNEL) method. Malondialdehyde (MDA) levels were determined in uterine tissue of rats. Fluoride caused a significant increase in NIDA levels (an important marker of lipid peroxidation) in the fluoride group compared with the controls (p < 0.05). Vitamins E and C significantly reduced the fluoride-induced lipid peroxidation in the F + Vit group compared with the F group (p < 0.05). Diffuse apoptosis in glandular epithelium and stromal cells was found in endometrial tissues of F treated rats by TUNEL method. The severity of these lesions was reduced by the administration of vitamins. From these results, it can be concluded that subchronic fluoride administration causes endometrial apoptosis, and lipid peroxidation may be a molecular mechanism involved in fluoride-induced toxicity. Furthermore, treatment with a combination of vitamins E and C reduced endometrial apoptosis caused by fluoride. (c) 2006 Elsevier Ireland Ltd. All rights reserved

Niclosamide Suppresses Proliferation, Induces Apoptosis and Inhibits Wnt/beta-catenin Signaling Pathway in Human Ovarian Cancer Cells

Objective: The aim of this study is to investigate in vitro effects of an antihelminthic drug niclosamide on human ovarian carcinoma cell line OVCAR3

Neuroprotective role of delta opioid receptors in hypoxic preconditioning

Background/aim: The purpose of the present study was to explore the neuroprotective role of delta opioid receptors (DOR) in the rat cortex in hypoxic preconditioning. Materials and methods: Rats were randomly divided into 8 groups: control (C), sham (5), hypoxic preconditioning (PC), severe hypoxia (SH), PC + SH, PC + SH + Saline (PS), PC + SH + DPDPE (DPDPE, selective DOR agonise), PC + SH + NT (NT, Naltrindole, selective DOR antagonist). Drugs were administered intracerebroventrically. Twenty four h after the end of 3 consecutive days of PC (10\% O-2 , 2 h/day), the rats were subjected to severe hypoxia (7\% O-2 for 3 h). Bcl-2 and cyt-c were measured by western blot, and caspase-3 was observed immunohistochemically. Results: Bcl-2 expressions in the PC group were higher than in control, SH, and PC + SH groups. Even though there were no significant differences between the groups in terms of cyt-c levels, caspase-3 immunoreactivity of cortical neurons and glial cells in the severe hypoxia and NT groups were higher than in the control, sham, and hypoxic preconditioning groups. DPDPE administration diminished caspase-3 immunoreactivity compared with all of the severe hypoxia groups. Conclusions: These results suggest that cortical cells are resistant to apoptosis via increased expression of Bcl-2 and decreased immunoreactivity of caspase-3 in the cortex, and that DOR is involved in neuroprotection induced by hypoxic preconditioning via the caspase-3 pathway in cortical neurons

Bacopa Monnieri Protects the Directly Affected Organ as Well as Distant Organs Against I/R Injury by Modulating Anti-Inflammatory and Anti-Nitrosative Pathways in A Rat Model for Infra-Renal Aortic Occlusion

Objective: To investigate the protective effect and underlying mechanisms of B. monnieri, a medicinal plant, on kidney and skeletal muscle injury induced by infra-renal abdominal aorta clamping for 2-hours (ischemia) and following removal of the clamp (reperfusion, 2-hours). Methods: Rats were divided into four groups (n = 6): (I) animals given only saline (sham-control); (II) animals given B. monnieri extract for 10-days (300 mg/kg/day) (Bacopa-treated sham); (III) animals subjected to ischemia/reperfusion (I/R); (IV) animals given B. monnieri extract and then subjected to I/R. Kidneys and lower extremity muscles were examined for GPx, CAT, iNOS, 3-NT, IL-1 beta and TNF-alpha. Apoptosis and injury were evaluated by TUNEL and H&E staining, respectively. Results: I/R resulted in TUNEL positive cells, periarterial edema and glomerular capillary dilatation, decreased GPx activity, unchanged CAT, iNOS, 3-NT, IL-1 beta and TNF-alpha in kidney. B. monnieri minimized renal remote reperfusion injury, and Group IV showed a lower degree of renal histopathology score when compared to the others. B. monnieri mitigated muscle I/R injury, decreased muscle hypertrophy, myofibril abnormalities and apoptosis. Muscle 3-NT and cytokine levels were increased by I/R, and B. monnieri inhibited iNOS and 3-NT both in sham-control and I/R groups. Muscle GPx unaffected by I/R or B. monnieri, but CAT was inhibited only in B. monnieri-treated I/R group. Muscle iNOS, 3-NT, IL-1 beta, TNF-alpha levels and CAT activity of B. monnieri-treated I/R rats were lower than those in sham-control or Bacopa-treated sham. Conclusions: B. monnieri can protect the directly affected organ as well as distant organs against I/R injury by modulating anti-inflammatory and anti-nitrosative pathways

Is leptin receptor expression triggered in the case of embryo transfer to endometrium coculture?

Background/aim: A synchronized dialogue between maternal and embryonic tissues is required for successful implantation. Low uterine receptivity is responsible for two-thirds of implantation failures and leptin is effective in the physiology of reproduction by binding to specific receptors. In this study, we investigateleptin receptor expression in cases of embryo transfer to endometrial coculture. Materials and methods: Biopsy materials were taken from 20 females with indication for coculture application and were cultured in an appropriate medium after the epithelial cells were isolated. The grown cells were cultured in chamber slides as the first group. For the second group, day 3 embryo was added to chamber slides and the development was observed. The embryo was transferred 1 or 2 days later and other cells (after the transfer process) were used to form the second group. After fixation, immunohistochemical staining was performed with anti-leptin primary antibody. Results: Regarding the coculture without embryo transfer, moderate leptin receptor immunoreactivity was seen in the perinuclear region and the cell membrane. Also, regarding the coculture with embryo transfer, moderate leptin receptor immunoreactivity was seen in the cytoplasm and strong leptin receptor immunoreactivity was seen in the cell membrane. Conclusion: Embryo transfer to endometrium coculture triggers leptin receptor expressio

Evaluation of caspase-dependent apoptosis during methyl parathion-induced endometrial damage in rats:: Ameliorating effect of Vitamins E and C

The role of reactive oxygen species (ROS) in various diseases of the female reproductive tract has been shown, and oxidative stress is an important component of the mechanism of toxicity of Opts. Methyl parathion (MPT) is one of the most widely used organophosphate insecticides (Opts) in agriculture. The aim of the study was to elucidate the effect of subchronic NIPT exposure on lipid peroxidation and serum activities of cholinesterase (ChE), and the protective effects of combination of antioxidant Vitamins E and C in rats. Additionally, histopathological and immunohistochemical changes in endometrium were aimed to be examined. Three groups of rats were used in the experiment. The first group was treated with 5 mg/kg NIPT; the second group Was treated with 5 mg/kg body weight NIPT plus Vitamin E and Vitamin C (NIPT + Vit) and the third group was given only corn oil (control). NIPT and NIPT + Vit groups were given MPT by gavage 5 days a week for 4 weeks at a dose level of 4 mg/(kg day) by using corn oil as the vechicle. Vitamins E and C were injected at doses of 50 mg/kg i.m. and 20 mg/kg body weight i.p. Histopathological and immunohistochemical examinations for caspase-3 and caspase-9 were accomplished in the endometrium. The level of malondialdehyde (NIDA) increased significantly in the NIPT group compared with the control group (p < 0.05). NIDA significantly decreased in the NIPT + Vit group compared with the MPT group (p < 0.05). Administration of Vitamins E and C along with NIPT significantly reduced the histopathological changes and the extent of apoptosis. In conclusion, subchronic NIPT administration caused endometrial damage and that treatment with a combination of Vitamins E and C reduced endometrial damage caused by NIPT. (c) 2006 Elsevier B.V. All rights reserved

Can Quercetin be an Option for Treatment of Spinal Cord Injury? An Experimental Study

AIM: To determine the neuroprotective functions of quercetin and compare them with methylprednisolone in an experimental spinal cord injury model in rats

Histological and electron microscopic examination of the effect of Dexketoprofen Trometamol on liver in rats

WOS: 000413375800008Background: The current study was performed for histological and electron microscopic examination of the effects of different doses of dexketoprofen trometamol on liver in rats. Material and Methods: Shame group consisted of rats administered 1 ml of 0.9% NaCl twice a day via intraperitoneal route, 8 mg/kg/day was used in Dexketoprofen Trometamol low-dose group, and 16 mg/kg/day was used in Dexketoprofen Trometamol high-dose group. 30 healthy Wistar albino type male rats were used in the study as animal materials. Results: The presence of TUNEL positive cells was increased with the increasing dose level of Dexketoprofen Trometamol and TUNEL positive hepatocytes distributed all over the tissue. Diffuse degeneration was determined in the liver sections of the group administered high-dose. Necrotic areas became more apparent particularly in regions close to the central vein. PCNA involvement was detected to be considerably increased compared to the shame and low-dose groups. Electron microscopic image of liver in the group administered high-dose drug showed that all hepatocytes present with highly active cell structure. Hepatocyte mitochondria were observed to be highly developed and to grow large and fuse from place to place. Granulated and smooth endoplasmic reticulum tubulus and cisternae displayed a highly-dilated appearance. Bile canaliculi were distinguished as dilated and its lumen was covered with microvilli. There were many vacuolar formation in addition to lipid droplets in the cytoplasms of ito cells. Conclusion: Dexketroprofen Trometamol drug administration was determined to increase activation particularly in parenchymal cells depending on dose and cause degeneration in liver tissue with heavy activity

Effect of Dexketoprofen Trometamol as Immunohistochemical and Electron Microscopy on Kidney in Rats

WOS: 000452553400004Background and Objective: Dexketoprofen trometamol is the dextrorotatory enantiomer of NSAID ketoprofen formulated as a tromethamine salt. This study aimed to perform immunohistochemical and electron microscopic evaluations of the effects of two different doses of dexketoprofen trometamol on kidneys via parenteral administration for 7 days. Materials and Methods: The study was conducted on 30 healthy, male Wistar albino rats, each weighing approximately 220 g. The rats were randomized and distributed across 3 groups, with 10 rats in each group. In the control group, 0.9% NaCl was used in 1 mL volume. In the other groups, and 16 mg kg(-1)/day doses of dexketoprofen trometamol (Arveles 50 mg/2 mL) in 1 mL were used intraperitoneally twice per day for 7 days. Results: In the high-dose group, a statistically significant reduction in live weight was observed, along with apoptosis and increased cell proliferation when compared to the control group. In the low-dose group, statistically significant increased apoptosis and cell proliferation were found. Conclusion: It was found that dexketoprofen trometamol induced apoptosis and caused cell proliferation and the 16 mg kg(-1)/day dose initiated the necrotic process. When an overdose of dexketoprofen trometamol (16 mg kg(-1)) was administered, losses in live weight and diffuse degeneration of the kidney tissue occurred. Administrations of this dosage are not recommended as similar effects on human tissue are predicted