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It is known that obesity is associated with a state of chronic low-level inflammation. Some data indicate that obesity- related stress could increase the hypothalamo-pituitary-adrenal axis activity. This leads to a rise in the plasma glucocorticoid level, which induces the development and differentiation of preadipocytes. Thus, the present study was performed to examine the effect of glucocorticoids on the expression of resistin and adiponectin mRNAs in adipose tissue during acute and chronic inflammation in mice. The results of the study showed an increase in the expression of resistin mRNA and a decrease in the expression of adiponectin mRNA during chronic inflammation (obese animals). Synthetic glucocorticoids changed the expression of both adipokines in a different manner according to the state of inflammation. To sum up, the action of glucocorticoids in adipose tissue depends on the immune system activity.
BACKGROUNDANDAIMS: The phenomenon of communication between the nervous and immune systems is commonly accepted. There were postulated several pathways for information exchange between these two systems, among them: neuronal with the vagus nerve, and enzymatic exercised through cyclooxygenases. The fact of biological compensation of many processes in our organisms is well known. In our project we hypothesized the existence of such phenomenon is situation of affected pathway for transferring of immune signal from the periphery to the brain after inhibition of cyclooxygenases. METHODS: To investigate the existence of these mechanisms, neurochemical changes occurring in the hypothalamus (the initial section of the stress axis – HPA) after intraperitoneal administration of LPS (10 mcg/animal) were analyzed. We studied the effect of long-term (10 days) administration of cyclooxygenases inhibitors on the neurochemical changes in the activity of the hypothalamus in response to LPS or saline ip administration. The rats were subcutaneously injected with selective cyclooxygenases inhibitors; Celecoxib (10 mg/kg) and SC-560 (3 mg/kg), respectively. RESULTS: Future HPLC analysis shown an increased activity of the noradrenergic and serotonergic systems within the hypothalamus. These data are comparable with those obtained after saline injections. CONCLUSIONS: These results suggest the presence of compensatory mechanisms responsible for the stimulation of the HPA axis after peripherally immune challenges. They also suggest that longterm intake of non-steroidal anti-inflammatory drugs may not affect, or in a very minor degree, the relationships between the immune and the nervous systems. Supported by NCN: UMO-2012/07/B/NZ4/00205.
BACKGROUND AND AIMS: Peripheral administration of gram-negative bacteria endotoxin – lipopolisaccharide (LPS) is known to activate the hypothalamo-pituitary adrenal axis (HPAA) and brain noradrenergic systems. We studied the vagotomized rats responses to peripherally administered LPS using the HPLC-ED to measure the concentration of noradrenaline and their metabolite MHPG in various brain regions. METHODS: Rats were submitted to subdiaphragmatic vagotomy and after 30 days we used them for experiments. They were injected with saline (100 μl ip) and LPS (10 μg/100 μl ip) in random order, and two hours after injection they were euthanized. They brains where removed from the skull and we isolated the hypothalamus, amygdala, prefrontal medial cortex, hippocampus periaqueductal gray matter and the brainstem and submitted for chromatographic analysis. RESULTS: Future chromatographic analysis indicates, that subdiaphragmatic vagotomy did not protect against increase of noradrenaline concentration in analyzed brain regions. In case of LPS injected animals we observed increased noradrenaline concentration versus saline injected ones. These results were comparable with those observed in sham operated rats. CONCLUSIONS: There results suggest that there may be compensatory mechanisms, responsible for transferring of immune signal to the brain, and develop during such a long time of recovery after subdiaphragmatic vagotomy. Supported by NCN, grant no. UMO-2012/07/B/NZ4/00205
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