Increased growth hormone secretagogue receptor-1a (GHSR-1a) in hypothalamus during olanzapine treatment in rats.

Weight gain is the one of the most important factors which increases global burden of psychiatric disorder. Second-generation antipsychotics, olanzapine (Olz) and valproic acid (Vpa) in particular, are held responsible for weight gain. However, it is still uncertain how these drugs cause this. Thus, the rats selected for the experiment were randomly divided into 3 groups. The 1st group received only 0.5 ml saline solution intraperitoneally (n = 20, control group); the second group was given 200 mg / kg Vpa intraperitoneally (n = 20, Vpa group) and 2 mg / kg Olz was given intraperitoneally to the 3rd group (n = 20, Olz group) between 8 and 10 am for 30 days. We examined serum leptin, adiponectin, resistin, TNF-α, IL-6, ghrelin level and, the amount of ghrelin secreting cells in the stomach and growth hormone secretagogue receptor-1a (GHSR-1a, ghrelin receptor) expression in the hypothalamus. The hypothalamic GHS-1a receptor index was significantly higher in the Olz group compared with the control group and Vpa group (p = 0.036 and p = 0.016 respectively). Ghrelin immune positive cell index in stomach was statistically significantly lower in the Vpa group compared with the control and Olz groups (p = 0.028 and p = 0.013 respectively) There was no difference between the groups in terms of serum leptin, resistin, IL-6 and ghrelin levels. In the Vpa group, a statistically significant increase was found in serum adiponectin level compared with both the control group and the Olz group (p = 0009 and p = 0024 respectively) and, significant decrease was found in serum TNF-α level compared to Olz group (p = 0007). In conclusion, we found that the main cause of weight gain in Olz use was the increase in the number of hypothalamic ghrelin receptors. Investigating the mechanism by which Olz increases the number of ghrelin receptors may help to develop effective treatment strategies in preventing obesity in psychiatric patients.

Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to 900 MHz electromagnetic fields.

PURPOSE: Adverse effects on human health caused by electromagnetic fields (EMF) associated with the use of mobile phones, particularly among young people, are increasing all the time. The potential deleterious effects of EMF exposure resulting from mobile phones being used in close proximity to the brain require particular evaluation. However, only a limited number of studies have investigated the effects of prenatal exposure to EMF in the development of the pyramidal cells using melatonin (MEL) and omega-3 (ω-3). MATERIALS AND METHODS: We established seven groups of pregnant rats consisting of three animals each; control (CONT), SHAM, EMF, EMF + MEL, MEL, EMF + ω-3 and ω-3 alone. The rats in the EMF, EMF + MEL, EMF + ω-3 groups were exposed to 900 MHz EMF for 60 min/day in an exposure tube during the gestation period. The CONT, MEL and ω-3 group rats were not placed inside the exposure tube or exposed to EMF during the study period. After delivery, only spontaneously delivered male rat pups were selected for the establishment of further groups. Each group of offspring consisted of six animals. The optical fractionator technique was used to determine total pyramidal neuron numbers in the rat hippocampal region. RESULTS: The total number of pyramidal cells in the cornu ammonis (CA) in the EMF group was significantly lower than in the CONT, SHAM, EMF + MEL, and EMF + ω-3 groups. No significant difference was observed between the EMF, MEL and ω-3 groups. No difference was also observed between any groups in terms of rats' body or brain weights. CONCLUSION: MEL and ω-3 can protect the cell against neuronal damage in the hippocampus induced by 900 MHz EMF. However, further studies are now needed to evaluate the chronic effects of 900 MHz EMF on the brain in the prenatal period.

A new hypothesis about neuronal degeneration appeared after a rat model of menopause.

OBJECTIVE: Estrogen is suggested to be one of the most important regulators of neuronal function, including neuronal proliferation, survival and plasticity. There is a broad consensus that the loss of ovarian hormones is associated with neurodegeneration in the hippocampus that leads to cognitive impairment. METHODS: A total of 8 female rats which were subjected to bilateral ovariectomy were included in this study. After ovariectomy, the rats were housed for 123 days in a standard laboratory. At the end of the 123 days, the rats were euthanized and the brain sections were investigated by conventional light microscopic and electron microscopic techniques. RESULTS: The regular structure of almost all axon extensions was lost. The majority of these extensions had a sawtooth-like appearance in longitudinal section profiles. Especially in transfer section profiles of myelinated axons, some morphological changes were shown which may be matched up with light microscopic findings. CONCLUSIONS: Deficiency of estrogen will initially affect microtubule organization. When this organization breaks down, it will physically cause the distribution of the normal structure of axonal plasmalemma. This in turn will lead to the distribution of physical organizations of estrogen and other different types of receptors which are placed in both the membrane and microtubules in the axon.

The effects of polymicrobial sepsis with diabetes mellitus on kidney tissues in ovariectomized rats.

OBJECTIVES: Sepsis model was used to understand the role of sustained hyperglycemia and ovariectomy, either separately or concomitantly, on the response of the activity of the nuclear factor kappa B (NF-kappaB) and the oxidative response in kidney. SUBJECTS: Polymicrobial sepsis was induced by cecal ligation and puncture (CLP). Diabetes was induced in female rats using administration of alloxan. The rats were divided into five groups: sham control (group 1), ovariectomy (group 2), ovariectomy + sepsis (group 3), ovariectomy + diabetes (group 4), and ovariectomy + diabetic + sepsis (group 5). RESULTS: In kidney tissues, the levels of lipid peroxidation (LPO) and glutathione (GSH) and the activity of catalase (CAT) were higher for groups 3, 4, 5 than the control groups. Superoxide dismutase (SOD) activity was lower for groups 3, 4, 5 than the control groups. We determined that CLP produced injury evident in the kidneys of rats when compared to the control group, whereas the severity of the injury was higher in the diabetes + ovariectomy + CLP group when compared to the CLP group. In immunohistochemical staining, we determined that CLP operation increased NF-kappaB activation. In the ovariectomized, septic, and diabetic group, NF-kappaB activation was significantly higher than other groups. CONCLUSIONS: Hyperglycemia and ovariectomy severely increased NF-kappaB activation and oxidant levels with the stages of our sepsis model. Ovariectomy resulted in general changes in metabolism, which are seen in the kidney with diabetes under sepsis conditions.

Effects of hypertension and ovariectomy on rat hepatocytes. Are amlodipine and lacidipine protective? (A stereological and histological study).

BACKGROUND/AIMS: Calcium channel blockers are increasingly used for the treatment of hypertension. Menopause and hypertension are both important risk factors for liver damage and several other circulatory abnormalities. The aim of this study was to determine the effects of amlodipine and lacidipine in an ovariectomy-induced postmenopausal period model and a deoxycorticosterone acetate-salt-induced hypertensive model in rats. METHODS: In this study, animals were divided into six groups as follows: control (Group 1), hypertension (Group 2), ovariectomy (Group 3), ovariectomy and hypertension (Group 4), ovariectomy, hypertension and amlodipine-treated (Group 5), and ovariectomy, hypertension and lacidipine-treated (Group 6). At the end of the experiment, the livers were removed and tissue samples were histologically and stereologically examined. RESULTS: The numerical densities of the hepatocytes according to group were 0.000422, 0.00329, 0.000272, 0.00259, 0.00374 and 0.000346 µm3, respectively. Significant differences were found between values of all groups (p<0.01, Mann-Whitney U test). According to histopathological investigation, Group 3 and particularly Group 4 showed some microscopic abnormalities such as dilatation in sinusoids central veins and branches of portal vein, irregularities of the hepatocyte columns, significant mononuclear cell infiltrations, and unstained vacuoles in the cytoplasm of the hepatocytes. Histological structure was protected from the destructive effects of ovariectomy and hypertension in Groups 5 and 6. CONCLUSIONS: Our experimental results show that both hypertension and the postmenopausal period have negative effects on the number of hepatocytes and histological structure of the liver. Both amlodipine and lacidipine appear to ameliorate the hypertension and/or postmenopausal period-related decrease in hepatocyte number. We thus suggest that lacidipine and particularly amlodipine have important protective and recovering effects on the liver.

Protective effects of telmisartan on ischemia/reperfusion injury of rat ovary: biochemical and histopathologic evaluation.

OBJECTIVE: To evaluate the effects of telmisartan as an antioxidant and for its tissue protective properties and to study the biochemical and histopathologic changes in experimental ischemia and ischemia/reperfusion injuries in rat ovaries. DESIGN: Experimental study. SETTING: Experimental surgery laboratory in a university department. ANIMAL(S): Forty-eight female adult rats. INTERVENTION(S): I: sham operation; II: bilateral ovarian ischemia; III: 3 h ischemia + 3 h reperfusion. IV and V: Rats were administered 10 and 20 mg/kg doses of telmisartan, respectively, before 0.5 h of ischemia, and then ovarian ischemia was applied; after 3 h of ischemia, the ovaries were removed. VI and VII: 3 h ovarian ischemia was applied; 2.5 h after the induction of ischemia, rats were administered the same doses of telmisartan; at the end of 3 h of ischemia, the ovaries were removed and a 3 h reperfusion followed. MAIN OUTCOME MEASURE(S): Superoxide dismutase, inducible nitric oxide synthase, and myeloperoxidase activity in rat ovarian tissue; and histopathologic changes in the ovarian tissue of the rats. RESULT(S): Ischemia and ischemia-reperfusion increased the inducible nitric oxide synthase and myeloperoxidase activity while decreasing the super oxide dismutase activity significantly in comparison with the sham group. Before ischemia and ischemia/reperfusion, telmisartan reversed the trend in inducible nitric oxide synthase activities and the level of myeloperoxidase. CONCLUSION(S): telmisartan is effective in reversing tissue damage induced by ischemia/reperfusion in ovaries.

Cytotoxic effects of TEGDMA on THP-1 cells in vitro.

OBJECTIVE: Resin based dental materials are not stable in the oral environment and may release their components into biological media. These components may include substances such as triethylene glycol dimethacrylate (TEGDMA), which is a major co-monomer of dental resin materials. This release can trigger host immune and inflammatory responses against foreign materials, mediated by monocytes. The aim of this study was to investigate the possible cytotoxic effects of TEGDMA on human THP-1 monocytes. MATERIAL AND METHODS: THP-1 cells were exposed to various concentrations of TEGDMA (0.5 mM, 1 mM, 2 mM, 4 mM, or 8 mM) for 48 hours. An untreated group was used as control. The effects of TEGDMA on cell proliferation, cell viability and apoptosis were analyzed by light microscopy. RESULTS: Cell proliferation was inhibited by 4 mM and 8 Mm TEGDMA. Increasing TEGDMA concentrations caused a decrease in cell viability. All TEGDMA concentrations used in this study had an apoptotic effect on THP-1 cells when compared with the control group. CONCLUSIONS: The dental monomer TEGDMA had an adverse effect on cell proliferation and exerted an apoptotic and toxic effect on THP-1 cells in a concentration-dependent manner.

Cytotoxic effects of TEGDMA on THP-1 cells in vitro

Objective: Resin based dental materials are not stable in the oral environment and may release their componentsinto biological media. These components may include substances such as triethylene glycol dimethacrylate(TEGDMA), which is a major co-monomer of dental resin materials. This release can trigger host immune andinflammatory responses against foreign materials, mediated by monocytes. The aim of this study was to investigatethe possible cytotoxic effects of TEGDMA on human THP-1 monocytes.Material and Methods: THP-1 cells were exposed to various concentrations of TEGDMA (0.5 mM, 1 mM, 2 mM,4 mM, or 8 mM) for 48 hours. An untreated group was used as control. The effects of TEGDMA on cell proliferation,cell viability and apoptosis were analyzed by light microscopy.Results: Cell proliferation was inhibited by 4 mM and 8 Mm TEGDMA. Increasing TEGDMA concentrationscaused a decrease in cell viability. All TEGDMA concentrations used in this study had an apoptotic effect onTHP-1 cells when compared with the control group.Conclusions: The dental monomer TEGDMA had an adverse effect on cell proliferation and exerted an apoptoticand toxic effect on THP-1 cells in a concentration-dependent manner (AU)

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