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1

Dual role of endogenous nitric oxide in development of dextran sulfate sodium-induced colitis in rats

100%

Rumi G., Tsubouchi R., Nishio H., Kato S., Mozsik G., Takeuchi K.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 4

The role of nitric oxide (NO) in the etiology of ulcerative colitis is controversial with reports of the improvement and aggravation of colonic lesions by inducible NO synthase (iNOS) inhibitors. In the present study, we compared the effect of the selective iNOS inhibitor aminoguanidine and the nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on a dextran sulfate sodium (DSS)-induced model of colitis in rats. Experimental colitis was induced by a 3% DSS-solution added to drinking water for 7 days. Aminoguanidine (5~20 mg/kg) and L-NAME (10 mg/kg) were administered p.o. twice daily for the first 3 days, the last 3 days or all 6 days of DSS treatment. Body weight and severity of colitis (diarrhea, bloody feces) were observed over a period of 7 days. DSS treatment resulted in severe colonic lesions, accompanied by diarrhea, bloody feces, decrease of body weight and colon shortening. All of the parameters investigated improved significantly with aminoguanidine treatment at 20 mg/kg for 6 days or the last 3 days of DSS-treatment, but L-NAME did not significantly affect the colitis during these periods. When L-NAME or aminoguanidine was given in the first 3 days of DSS treatment, the colonic lesions were slightly aggravated by L-NAME but not affected by aminoguanidine. The expression of iNOS mRNA was observed from the 3rd day of DSS treatment. These results suggested that endogenous NO exerts a biphasic influence on DSS-induced colitis, depending on the NOS isoenzyme; a beneficial effect of NO derived from constitutive NOS and a detrimental effect of NO produced by iNOS in the development of colitis.

2

Psychosocial stress affects the involvement of prostaglandins and nitric oxide in the lipopolysaccharide-induced hypothalamic-pituitary-adrenal response

100%

Gadek-Michalska A., Spyrka J., Bugajski J.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 2

The role of prostaglandins and nitric oxide (NO), generated after peripheral lipopolysaccharide (LPS) administration, in the adaptation of hypothalamic-pituitary-adrenal (HPA) axis under stressful circumstances remains to be elucidated. The aim of the present study was to assess the effect of chronic repetitive restraint or social crowding stress on the involvememt of nitric oxide and prostaglandins in the LPS-induced pituitary-adrenocortical response. Male Wistar rats were restrained in metal tubes 2x10 min/day or crowded in cages for 7 days prior to treatment. All compounds were injected i.p., cyclooxygenase (COX) and nitric oxide synthase (NOS) inhibitors 15 min before LPS. Two hrs after injection LPS induced a significant increase in ACTH and corticosterone secretion. Repeated restraint impaired more potently than crowding stress the LPS-induced HPA-response. Indomethacin, a non-selective COX inhibitor, considerably reduced the LPS-induced HPA response in non-stressed rats and to a lesser extent diminished this response in repeatedly restrained or crowded rats. Neuronal NOS inhibitor, Nw-nitro-L-arginine decreased the LPS-induced HPA response, more potently in control than crowded rats. Aminoguanidine, an iNOS inhibitor, diminished the LPS-elicited ACTH response in crowded rats. These results indicate that prostaglandins and NO generated by neuronal and inducible NOS are involved in the LPS-induced HPA axis response under basal conditions and during its adaptation to chronic social stress circumstances.

3

Blockade of nitric oxide formation in the rat brain does not disturb development of endotoxin tolerance

84%

Soszynski D., Daniluk M., Galazka M., Dmitruk K.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 6

4

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Role of polyamines in gastroprotection induced by epidermal growth factor

84%

Brzozowski T., Drozdowicz D., Majka J., Polonczyk-Pytko J., Konturek S. J.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 2

Polyamines have been shown to stimulate cellular growth and differentiation, though their role in the prevention of acute gastric lesion induced by various noxious agents has been little studied. Epidermal growth factor (EGF) exhibits gastroprotective and ulcer healing properties due to its potent mitogenic and growth promoting action. This study was designed to compare the gastroprotective effects of spermine and EGF against gastric damage induced by absolute ethanol, acidified aspirin and stress and to determine the role of endogenous polyamines in EGF-induced gast- troprotection. Spermine and EGF significantly reduced the lesions induced by all three ulcerogens. Oral administration of spermine or subcutaneous infusion of EGF in 24 h fasted rats with chronic gastric fistula resulted in similar inhibition of gastric acid and pepsin secretion. Pretreatment with difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase (ODC), a hey enzyme in the biosynthesis of polyamines, did not affect ethanol lesions, but reversed the protective effect EGF but not spermine, against ethanol. This finding indicates that polyamines mediate, at least in part, EGF-induced gastroprotection. In tests with oral administration of aminoguanidine that is known to suppress the activity of diamino-oxidase (DAO) and to inhibit the degradation of polyamines, EGF showed a markedly enhanced gastroprotective activity against ethanol damage. Since indomethacin failed to affect the gastroprotective effects of spermine and EOF and neither of these agents influenced the mucosal generation of PGE₂ in intact or injured gastric mucosa, we conclude that prostaglandins are not the major factors in spermine- and EGF-induced gastroprotection. This study demonstrates that polyamines are highly effective against gastric lesions induced by various ulcerogens and that they act as primary mediators of EGF-induced gastroprotection.

5

Bioelectrical activity of the amygdala of rats under conditions of chronic alcoholism and imbalance of nitric oxide

84%

Severynovska O., Babicheva V., Galinskiiy A., Rudenko A., Bogatyreva O., Boyko M.

International Letters of Natural Sciences

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2015

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tom 49

Evaluation of biopotentials in the region of the amygdala of rats in the combined influence of alcohol and drugs, causing an imbalance of nitric oxide is described in this paper. Chronic alcoholism leads to structural morphological changes in the liver. A study of the amplitude of electrical activity showed that the electrical potential in the amygdala after 8 weeks chronic alcoholism was lower compared with normal rats. The frequency spectrum analysis showed decreased in the 2 times or more absolute spectral powers of all components. The relative spectral powers of its components: δ: θ: α: β was as a 2: 2: 2: 4. The use of sodium nitroprusside (donator of NO) together with the chronic consumption of ethanol reduces the effect of ethanol on low and high-frequence portion the performance of the bioelectrical activities spectrum in the amygdala. The use of non-selective blocker of NO-synthase – nitroarginine aggravated by the braking action of alcohol. The important role of nitric oxide in the development of adaptive-compensatory reactions of the damaged body is described. Our results may be useful to assess the contribution of NO in operation amygdala, conditions of chronic pathologies, and treatment of neuropsychiatric conditions, including diseases caused by alcohol abuse.

6

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors attenuates fever due to LPS in rats

84%

Soszynski D., Chelminiak M.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

Nitric oxide (NO) has been shown to be an important mediator of febrile response to lipopolisaccharide (LPS). To clarify the role of different isoforms of NO synthase (NOS) in febrile response to immune challenge, effects of selective iNOS and nNOS inhibitors on fever to LPS were examined in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine (vL-NIO), a neuronal nitric oxide synthase (nNOS) inhibitor, and aminoguanidine hydrochloride, an inducible nitric oxide synthase (iNOS) inhibitor, were injected intracerebroventricularly at a dose of 10 µg/rat just before intraperitoneal injection of LPS at a dose of 50 µg/kg. Both inhibitors injected at a selected doses had no effect on normal day-time body temperature (Tb) and normal night-time Tb. vinyl-L-NIO and aminoguanidine injected intracerebroventricularly at a dose of 10 µg/animal suppressed the LPS-induced fever in rats. The fever index calculated for rats pretreated with v-LNIO or with aminoguanidine and injected with LPS was reduced by 43% and 72%, respectively, compared to that calculated for water-pretreated and LPS-injected rats. Whereas vL-NIO partly attenuated both phases of febrile rise in Tb, administration of aminoguanidine into the brain completely prevented fever induced by LPS. These data indicate that activation of iNOS inside the brain is not only responsible for triggering but also for maintaining of LPS-induced fever in rats. It is, therefore, reasonable to hypothesize that, activation of iNOS inside the brain is more important in fever development than activation of nNOS.

7

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors does not influence febrile response in rats during turpentine abscess

84%

Soszynski D., Chelminiak M.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

The purpose of this study was to investigate the role of neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) in the brain during development of fever in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. To determine the role of both NOSs in turpentine-induced fever, we injected vinyl-L-NIO (N5 – (1-Imino-3-butenyl) – ornithine (vL-NIO), a selective nNOS inhibitor, and aminoguanidine hydrochloride, a selective iNOS inhibitor, intracerebroventricularly (i.c.v.) 5 h after turpentine injection. Rats responded with fever to intramuscular injection of 20 µl of turpentine that commenced about 5 - 6 h after injection and reached peak value between 9 - 11 h post-turpentine. The inhibition of nNOS as well as iNOS in the brain did not affect fever induced by turpentine. Fevers in control rats (treated i.c.v. with pyrogen-free water) and iNOS or nNOS inhibitor-i.c.v. treated rats injected with turpentine were essentially the same. Furthermore, on the basis of these data, we concluded that iNOS and nNOS inside the brain do not participate in generation of fever to turpentine in rats.

8

EPR investigation of in vivo inhibitory effect of guanidine compounds on nitric oxide production in rat tissues

84%

Dambrova M., Kirjanova O., Baumane L., Liepinsh E., Zvejniece L., Muceniece R., Kalvinsh I., Wikberg J. E. S.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

The aim of the present study was to evaluate in vivo effects on NO production of pharmacologically widely used, commercially available NOS inhibitors, structurally related to guanidine. We compared the NO inhibitory potency and selectivity of L-NAME, aminoguanidine and guanabenz in tissues of normal and LPS-stimulated rats using ex vivo EPR measurements of the NO radical in its complex with dithiocarbamate-Fe(II). The tissues studied were the brain cortex, kidney, liver, heart and testis. Differential inhibitory effects were seen for L-NAME, aminoguanidine and guanabenz when applied during basal or LPS-stimulated conditions. Aminoguanidine exerted inhibition of NO only after stimulation with LPS. Guanabenz had little effect on NO in liver, kidney, testis and heart under normal conditions, while it reduced the basal NO in brain cortex. After stimulation with LPS guanabenz afforded a partial inhibition of the NO formation in all tissues studied. L-NAME was a potent inhibitor of NO synthesis in all tested tissues, both during basal and LPS stimulated conditions. Our results show that compounds containing a guanidine moiety might possess different NOS inhibitory profiles in vivo.

9

Molecular mechanism of emotional fever - the role of nitric oxide

67%

Soszynski D.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 8

51-59

The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 µg and 10 µg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in Tb and it was accompanied with an increase of motor activity. Both inhibitors significantly suppressed the stress fever. vL-NIO did not influence stress-induced rise in locomotor activity as well as did not change Tb in unstressed rats. Since aminoguanidine caused a transient fall in Tb below the baseline in rats exposed or not to open field and because this inhibitor suppressed stress-induced rise in locomotor activity, we concluded that nNOS expression inside the brain is critically involved in the rise in Tb due to exposure to psychological stress.

10

Effect of aminoguanidine and albendazole on inducible nitric oxide synthase [iNOS] activity in T.spiralis-infected mice muscles

67%

Zeromski J., Boczon K., Wandurska-Nowak E., Mozer-Lisewska I.

Folia Histochemica et Cytobiologica

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2005

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tom 43

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nr 3

Ograniczanie wyników

Dual role of endogenous nitric oxide in development of dextran sulfate sodium-induced colitis in rats

Psychosocial stress affects the involvement of prostaglandins and nitric oxide in the lipopolysaccharide-induced hypothalamic-pituitary-adrenal response

Blockade of nitric oxide formation in the rat brain does not disturb development of endotoxin tolerance

Role of polyamines in gastroprotection induced by epidermal growth factor

Bioelectrical activity of the amygdala of rats under conditions of chronic alcoholism and imbalance of nitric oxide

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors attenuates fever due to LPS in rats

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors does not influence febrile response in rats during turpentine abscess

EPR investigation of in vivo inhibitory effect of guanidine compounds on nitric oxide production in rat tissues

Molecular mechanism of emotional fever - the role of nitric oxide

Effect of aminoguanidine and albendazole on inducible nitric oxide synthase [iNOS] activity in T.spiralis-infected mice muscles