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Id: lil-778343
Autor: Carvalho-Costa, P G; Branco, L G S; Leite-Panissi, C R A.
Título: Activation of locus coeruleus heme oxygenase-carbon monoxide pathway promoted an anxiolytic-like effect in rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;49(5):e5135, 2016. graf.
Idioma: en.
Projeto: CAPES/PROEX, FAPESP; . CAPES. L.G.S. Branco; . C.R.A. Leite-Panissi.
Resumo: The heme oxygenase-carbon monoxide pathway has been shown to play an important role in many physiological processes and is capable of altering nociception modulation in the nervous system by stimulating soluble guanylate cyclase (sGC). In the central nervous system, the locus coeruleus (LC) is known to be a region that expresses the heme oxygenase enzyme (HO), which catalyzes the metabolism of heme to carbon monoxide (CO). Additionally, several lines of evidence have suggested that the LC can be involved in the modulation of emotional states such as fear and anxiety. The purpose of this investigation was to evaluate the activation of the heme oxygenase-carbon monoxide pathway in the LC in the modulation of anxiety by using the elevated plus maze test (EPM) and light-dark box test (LDB) in rats. Experiments were performed on adult male Wistar rats weighing 250-300 g (n=182). The results showed that the intra-LC microinjection of heme-lysinate (600 nmol), a substrate for the enzyme HO, increased the number of entries into the open arms and the percentage of time spent in open arms in the elevated plus maze test, indicating a decrease in anxiety. Additionally, in the LDB test, intra-LC administration of heme-lysinate promoted an increase on time spent in the light compartment of the box. The intracerebroventricular microinjection of guanylate cyclase, an sGC inhibitor followed by the intra-LC microinjection of the heme-lysinate blocked the anxiolytic-like reaction on the EPM test and LDB test. It can therefore be concluded that CO in the LC produced by the HO pathway and acting via cGMP plays an anxiolytic-like role in the LC of rats.
Descritores: Ansiolíticos/farmacologia
Ansiedade/metabolismo
Comportamento Animal/efeitos dos fármacos
Monóxido de Carbono/metabolismo
Heme Oxigenase (Desciclizante)/metabolismo
Locus Cerúleo/metabolismo
Transdução de Sinais/fisiologia
-Monóxido de Carbono/fisiologia
Guanilato Ciclase/metabolismo
Locus Cerúleo/efeitos dos fármacos
Locus Cerúleo/fisiologia
Aprendizagem em Labirinto
Ratos Wistar
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  2 / 9 LILACS  
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Id: lil-766151
Autor: Jaarin, Kamsiah; Foong, Wai Dic; Yeoh, Min Hui; Kamarul, Zaman Yusoff Nik; Qodriyah, Haji Mohd Saad; Azman, Abdullah; Zuhair, Japar Sidik Fadhlullah; Juliana, Abdul Hamid; Kamisah, Yusof.
Título: Mechanisms of the antihypertensive effects of Nigella sativa oil in L-NAME-induced hypertensive rats
Fonte: Clinics;70(11):751-757, Nov. 2015. tab, graf.
Idioma: en.
Projeto: Universiti Kebangsaan Malaysia.
Resumo: OBJECTIVES: This study was conducted to determine whether the blood pressure-lowering effect of Nigella sativa might be mediated by its effects on nitric oxide, angiotensin-converting enzyme, heme oxygenase and oxidative stress markers. METHODS: Twenty-four adult male Sprague-Dawley rats were divided equally into 4 groups. One group served as the control (group 1), whereas the other three groups (groups 2-4) were administered L-NAME (25 mg/kg, intraperitoneally). Groups 3 and 4 were given oral nicardipine daily at a dose of 3 mg/kg and Nigella sativa oil at a dose of 2.5 mg/kg for 8 weeks, respectively, concomitantly with L-NAME administration. RESULTS: Nigella sativa oil prevented the increase in systolic blood pressure in the L-NAME-treated rats. The blood pressure reduction was associated with a reduction in cardiac lipid peroxidation product, NADPH oxidase, angiotensin-converting enzyme activity and plasma nitric oxide, as well as with an increase in heme oxygenase-1 activity in the heart. The effects of Nigella sativa on blood pressure, lipid peroxidation product, nicotinamide adenine dinucleotide phosphate oxidase and angiotensin-converting enzyme were similar to those of nicardipine. In contrast, L-NAME had opposite effects on lipid peroxidation, angiotensin-converting enzyme and NO. CONCLUSION: The antihypertensive effect of Nigella sativa oil appears to be mediated by a reduction in cardiac oxidative stress and angiotensin-converting enzyme activity, an increase in cardiac heme oxygenase-1 activity and a prevention of plasma nitric oxide loss. Thus, Nigella sativa oil might be beneficial for controlling hypertension.
Descritores: Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Hipertensão/tratamento farmacológico
Nigella sativa/química
Óleos Vegetais/farmacologia
-Anti-Hipertensivos/administração & dosagem
Heme Oxigenase (Desciclizante)/metabolismo
Hipertensão/induzido quimicamente
Modelos Animais
Malondialdeído/análise
NADPH Oxidases/metabolismo
NG-Nitroarginina Metil Éster
Nicardipino/administração & dosagem
Nicardipino/farmacologia
Óxido Nítrico/sangue
Estresse Oxidativo/efeitos dos fármacos
Peptidil Dipeptidase A/metabolismo
Ratos Sprague-Dawley
Limites: Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 9 LILACS  
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Id: lil-727658
Autor: Carvalho-Costa, P.G.; Branco, L.G.S.; Leite-Panissi, C.R.A..
Título: Acute stress-induced antinociception is cGMP-dependent but heme oxygenase-independent
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;47(12):1057-1061, 12/2014. graf.
Idioma: en.
Projeto: CAPES/PROEX, FAPESP; . CNPq.
Resumo: Endogenous carbon monoxide (CO), which is produced by the enzyme heme oxygenase (HO), participates as a neuromodulator in physiological processes such as thermoregulation and nociception by stimulating the formation of 3′,5′-cyclic guanosine monophosphate (cGMP). In particular, the acute physical restraint-induced fever of rats can be blocked by inhibiting the enzyme HO. A previous study reported that the HO-CO-cGMP pathway plays a key phasic antinociceptive role in modulating noninflammatory acute pain. Thus, this study evaluated the involvement of the HO-CO-cGMP pathway in antinociception induced by acute stress in male Wistar rats (250-300 g; n=8/group) using the analgesia index (AI) in the tail flick test. The results showed that antinociception induced by acute stress was not dependent on the HO-CO-cGMP pathway, as neither treatment with the HO inhibitor ZnDBPG nor heme-lysinate altered the AI. However, antinociception was dependent on cGMP activity because pretreatment with the guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (ODQ) blocked the increase in the AI induced by acute stress.
Descritores: Dor Aguda/prevenção & controle
Monóxido de Carbono/metabolismo
GMP Cíclico/metabolismo
Heme Oxigenase (Desciclizante)/metabolismo
Dor Nociceptiva/prevenção & controle
Transtornos de Estresse Traumático Agudo/metabolismo
-GMP Cíclico/antagonistas & inibidores
Deuteroporfirinas/metabolismo
Heme Oxigenase (Desciclizante)/antagonistas & inibidores
Heme/análogos & derivados
Heme/metabolismo
Lisina/análogos & derivados
Lisina/metabolismo
Dor Nociceptiva/metabolismo
Oxidiazóis/farmacologia
Medição da Dor/métodos
Ratos Wistar
Transdução de Sinais/fisiologia
Limites: Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  4 / 9 LILACS  
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Id: lil-541101
Autor: Shi, J; Mei, W; Yang, J.
Título: Heme metabolism enzymes are dynamically expressed during Xenopus embryonic development
Fonte: Biocell;32(3):259-263, Dec. 2008. ilus, tab.
Idioma: en.
Resumo: As the key component of many hemoproteins (heme-containing proteins), heme is involved in a broad range of biological processes. Enzymes required for heme biosynthesis and degradation pathways are evolutionarily conserved. While heme metabolism has been studied extensively, the expression of heme metabolism enzymes during development has not been described. Here, we report that all heme biosynthases and two heme oxygenases, which initiate heme degradation, are dynamically expressed during Xenopus embryonic development. All heme synthases, with the exception of aminolevulinic acid synthase 2, are maternally expressed. At neurula stage, heme synthases are expressed in the developing neural tissue and in migrating neural crest cells. At the swimming tadpole stage, expression of heme synthases can be detected in multiple lineages, including eyes, neural crest cells, developing central nervous system, ventral blood island, pronephron, and pronephric tubule. Similar to heme synthases, heme oxygenases are expressed maternally. Zygotic expression of heme oxygenases is mainly restricted to the developing neural and neural crest lineages. Unlike heme synthases, heme oxygenases are not expressed in the ventral blood island and are expressed at a very low level in the pronephron and pronephric tubule. This indicates that heme metabolism may play important roles during development.
Descritores: Desenvolvimento Embrionário
Embrião não Mamífero/anatomia & histologia
Embrião não Mamífero/fisiologia
Ferroquelatase/genética
Ferroquelatase/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
-Heme/genética
Heme/metabolismo
Heme Oxigenase (Desciclizante)/genética
Heme Oxigenase (Desciclizante)/metabolismo
Hibridização In Situ
Proteínas de Xenopus/genética
Proteínas de Xenopus/metabolismo
Xenopus/embriologia
Xenopus/genética
Xenopus/metabolismo
Limites: Seres Humanos
Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: AR40.1 - Biblioteca de la Facultad de Ciencias Médicas de la UNCuyo


  5 / 9 LILACS  
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Id: lil-505420
Autor: Nascimento, C. G. O; Branco, L. G. S.
Título: Antinociception synergy between the peripheral and spinal sites of the heme oxygenase-carbon monoxide pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(1):141-147, Jan. 2009. graf.
Idioma: en.
Conferência: Apresentado em: Miguel R. Covian Symposium, 4, Ribeirão Preto, May 23-25, 2008.
Resumo: We have shown that the peripheral and spinal cord heme oxygenase (HO)-carbon monoxide (CO)-soluble guanylate cyclase-cGMP pathways play an important role in antinociception in the rat experimental formalin model. Our objective was to determine if there is synergism between peripheral (paw) and spinal HO-CO pathways in nociception. Rats were handled and adapted to the experimental environment for a few days before the formalin test, in which 50 µL of a 1 percent formalin was injected subcutaneously into the dorsal surface of the right hind paw. The animals were then observed for 1 h and the frequency of flinching behavior was taken to represent the nociceptive response. Thirty minutes before the test, rats were pretreated with intrathecal injections of the HO inhibitor, zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) or heme-lysinate, which is a substrate of the HO pathway. The paw treatments took place 20 min before the test. Low doses of ZnDPBG did not increase nociception, while a low heme-lysinate dose did not change flinching behavior after paw or spinal injections. Combined subactive spinal (50 nmol) and peripheral (40 nmol) low doses of ZnDPBG induced hypernociception (increase of 80 percent in the first and 25 percent in the second phase flinching), whereas combined spinal-peripheral heme-lysinate (50 and 30 nmol) led to second phase antinociception (40 percent reduction in flinching). These findings suggest a synergy between the peripheral and spinal HO-CO pathways. Local activation of the HO system probably regulates the nociception initiation in peripheral tissue and participates in buffering the emerging nociceptive signals at the peripheral and spinal sites of action. In short, an antinociceptive synergy exists between peripheral and spinal HO pathways, which may reduce the doses required and side effects.
Descritores: Monóxido de Carbono/metabolismo
Guanilato Ciclase/administração & dosagem
Heme Oxigenase (Desciclizante)/metabolismo
Nociceptores/efeitos dos fármacos
Medição da Dor/efeitos dos fármacos
Receptores Citoplasmáticos e Nucleares/administração & dosagem
Medula Espinal/efeitos dos fármacos
-Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Guanilato Ciclase/farmacologia
Heme Oxigenase (Desciclizante)/efeitos dos fármacos
Injeções Espinhais
Nociceptores/fisiologia
Ratos Wistar
Transdução de Sinais
Medula Espinal/fisiologia
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  6 / 9 LILACS  
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Id: lil-394648
Autor: Neiva, Luciana Barros de Moura.
Título: O papel da heme oxigenase-1 na lesão celular desencadeada pelo sulfato de polimixina B em células LLC-PK1 / The role of heme oxygenase-1 in the cellular injury caused by polymyxin B sulphate on LLC-PK1 cells.
Fonte: São Paulo; s.n; 2004. 64 p. tab, graf.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Escola de Enfermagem para obtenção do grau de Mestre.
Resumo: A heme-oxigenase-1 (HO-1) é uma enzima induzível envolvida na degradação do grupo prostético heme, produzindo compostos com funções anti-oxidante, anti-inflamatória, anti-apoptótica e modulatória do sistema imune no rim. A importância de sua indução está associada à resposta adaptativa ao estresse oxidativo e à inflamação envolvidos na gênese da insuficiência renal aguda. O sulfato de polimixina B é um antibiótico usado no tratamento de infecções Gram-negativas e que apresenta um efeito nefrotóxico ainda não completamente elucidado. O objetivo deste estudo foi verificar a viabilidade e apoptose de células LLC-PK1 submetidas ao tratamento com polimixina B, com tempos de exposição diferentes, e pré-tratadas com hemin (indutor de heme oxigenase-1) ou protoporfirina de zinco (inibidor de heme oxigenase-1). Células renais de porco, LLC-PK1, foram cultivadas com polimixina B durante 24, 48 e 72 horas. A apoptose e viabilidade celular foram avaliadas usando diferentes doses do antibiótico: Controle (CTL, 0 µM); G1 (12,5µM); G2 (37,5µM); G3 (75µM); G4 (125µM) e G5 (375µM). O hemin (25µM) e a protoporfirina de zinco (10µM) foram administrados uma hora antes da polimixina B. Foram utilizados os métodos Acridine orange/ brometo de etídio (viabilidade) e Hoescht 33342 (apoptose). Os resultados demonstraram redução linear de viabilidade induzida pela polimixina B quando a dose e o tempo de exposição foram aumentados, isto foi confirmado pela variação inversa de apoptose. O hemin aumentou a viabilidade e reduziu apoptose na presença de polimixina B, sugerindo um efeito protetor da HO-1 neste modelo. O efeito observado para a protoporfirina de zinco foi semelhante ao descrito para o hemin. O estudo confirmou a citotoxicidade da polimixina B em células renais e constatou que esse efeito pode ser mediado pela HO-1 considerando o efeito obtido no tratamento com o indutor daquela enzima
Descritores: Lesão Renal Aguda
Células LLC-PK1/metabolismo
Heme Oxigenase (Desciclizante)/uso terapêutico
Rim
Polimixina B
-Lesão Renal Aguda
Análise de Variância
Responsável: BR41.1 - Biblioteca Wanda de Aguiar Horta
BR41.1; T2601


  7 / 9 LILACS  
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Id: lil-248436
Autor: Demple, B.
Título: Genetic responses against nitric oxide toxicity
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;32(11):1417-27, Nov. 1999. ilus, graf.
Idioma: en.
Conferência: Apresentado em: Meeting NO Brazil, Basic and Clinical Aspects of Nitric Oxide, Foz do Iguaçú, March. 10-13, 1999.
Resumo: The threat of free radical damage is opposed by coordinated responses that modulate expression of sets of gene products. In mammalian cells, 12 proteins are induced by exposure to nitric oxide (NO) levels that are sub-toxic but exceed the level needed to activate guanylate cyclase. Heme oxygenase 1 (HO-1) synthesis increases substantially, due to a 30- to 70-fold increase in the level of HO-1 mRNA. HO-1 induction is cGMP-independent and occurs mainly through increased mRNA stability, which therefore indicates a new NO-signaling pathway. HO-1 induction contributes to dramatically increased NO resistance and, together with the other inducible functions, constitutes an adaptive resistance pathway that also defends against oxidants such as H2O2. In E. coli, an oxidative stress response, the soxRS regulon, is activated by direct exposure of E. coli to NO, or by NO generated in murine macrophages after phagocytosis of the bacteria. This response is governed by the SoxR protein, a homodimeric transcription factor (17-kDa subunits) containing [2Fe-2S] clusters essential for its activity. SoxR responds to superoxide stress through one-electron oxidation of the iron-sulfur centers, but such oxidation is not observed in reactions of NO with SoxR. Instead, NO nitrosylates the iron-sulfur centers of SoxR both in vitro and in intact cells, which yields a form of the protein with maximal transcriptional activity. Although nitrosylated SoxR is very stable in purified form, the spectroscopic signals for the nitrosylated iron-sulfur centers disappear rapidly in vivo, indicating an active process to reverse or eliminate them.
Descritores: Heme Oxigenase (Desciclizante)
Óxido Nítrico/fisiologia
Fatores de Transcrição
Transcrição Genética
-Expressão Gênica
Óxido Nítrico/toxicidade
Estresse Oxidativo
Limites: Seres Humanos
Animais
Tipo de Publ: Revisão
Research Support, U.S. Gov't, P.H.S.
Responsável: BR1.1 - BIREME


  8 / 9 LILACS  
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Colombari, E
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Id: lil-226206
Autor: Johnson, R. A; Kozma, F; Colombari, E.
Título: Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;32(1):1-14, Jan. 1999.
Idioma: en.
Conferência: Apresentado em: Annual Meeting of the Federaçäo de Sociedades de Biologia Experimental, 13, Caxambu, Aug. 26-29, 1998.
Resumo: Carbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure
Descritores: Monóxido de Carbono/metabolismo
Fenômenos Fisiológicos Cardiovasculares
Heme Oxigenase (Desciclizante)/metabolismo
Heme/metabolismo
Músculo Liso Vascular/metabolismo
Núcleo Solitário/metabolismo
-Pressão Sanguínea/fisiologia
Vasoconstrição
Vasodilatação
Limites: Seres Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


  9 / 9 LILACS  
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Id: lil-86929
Autor: Kleiman de Pisarev, Diana L; Ferramola de Sancovich, Ana Maria; Sancovich, Horacio A.
Título: Effect of triiodothyronine in the regulation of haem biosynthetic pathway
Fonte: Acta physiol. pharmacol. latinoam;38(3):301-8, 1988. tab.
Idioma: en.
Resumo: La administración de triyodotironina a animales tiroidectomizados, disminuyó en un 50% el contenido de citocromo P-450. La actividad de hemo oxigenasa no se modificó por el tratamiento con triyodotironina, ya sea solo o con una dosis subóptima de Cl2Co. Bajo las mismas condiciones la actividad de la amino levulínico sintelasa no fue afectada. La triyodotironina produjo un incremento del 100% en la actividad de triptófano pirrolasa. Tanto la holo como la enzima total fueron aumentadas en el mismo grado. La actividad de la porfobilinógeno deaminasa-uroporfirinógeno co-sintetasa, fue inducida en los animales tratados con triyodotironina, en un 67% por sobre los valores de los animales tiroidectomizadosm y sólo 32% con respecto a los animales con operación simulada. Nuestros resultados sugieren que bajo estimulación por triyodotironina, la disminución en el contenido de citocromo P-450 no es debida a un aumento en la velocidad de degradación del hemo, sino a una disociación de éste para incrementar el "pool" celular del hemo, y saturar en parte a la nueva apotriptófano pirrolasa sintetizada
Descritores: 5-Aminolevulinato Sintetase/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Heme Oxigenase (Desciclizante)/metabolismo
Fígado/enzimologia
Oxigenases de Função Mista/metabolismo
Tri-Iodotironina/farmacologia
Triptofano Oxigenase/metabolismo
-Ratos Endogâmicos
Tireoidectomia
Limites: Ratos
Animais
Masculino
Responsável: BR1.1 - BIREME



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