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Physiological and Biochemical Responses of Three Echinacea Species to Salinity StressSabra, Ali 04 1900 (has links)
To determine the level of salt tolerance of the medicinal plant Echinacea, the physiological and biochemical characteristics of E. purpurea, E. pallida and E. angustifolia exposed to different NaCl levels (0, 50, 75, and 100 mM) were evaluated under hydroponic culture. Dry weights of shoots and roots were not affected by salinity; however E. purpurea and E. pallida exhibited higher survival rate than E. angustifolia, which also showed high salt injury index and electrolyte leakage compared to the other two species. Gas exchange (photosynthetic rate, stomatal conductance, and transpiration rate) showed a decline with increasing salt concentrations in all species with a more pronounced reduction in E. angustifolia. E. purpurea was able to retain more Na+ in the roots than the other two species showing its capacity to regulate Na+ translocation to shoots (Na+ exclusion). Moreover, the activities of two major antioxidant enzymes; superoxide dismutase (SOD) and ascorbate peroxidase (APX) were increased by salinity in E purperea, while the activities were decreased in E. angustifolia. The characteristic phytochemical profiles of caffeic acid derivatives (CADs) and alkamides/ketones were obtained for the three species, and quantitative changes were determined. Cichoric acid, the major CAD in E. purpurea, was increased with salinity up to 75 mM NaCl. A relative increase in alkamides and CADs was recorded in E. angustifolia, while in E. pallida, the level of echinacoside and major ketones (22 and 24) decreased, suggesting that the medicinal value of this species was compromised by salt stress. First evidence of salt-induced changes in alkamides and ketones in Echinacea was demonstrated in this study. Activity of phenylalanine ammonia-lyase (PAL), the major enzyme involved in the biosynthesis of CADs, was increased only in the roots of E. purpurea, further reflecting the differences in salt tolerance between species. It can be concluded that Echinacea species exhibited a limited degree of salt tolerance; however, E. purpurea showed a higher tolerance than E. pallida and E. angustifolia. This tolerance was mainly attributed to the increase in Na+ exclusion capacity, antioxidant activities and PAL activity.
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Physiological and Biochemical Responses of Three Echinacea Species to Salinity StressSabra, Ali 04 1900 (has links)
To determine the level of salt tolerance of the medicinal plant Echinacea, the physiological and biochemical characteristics of E. purpurea, E. pallida and E. angustifolia exposed to different NaCl levels (0, 50, 75, and 100 mM) were evaluated under hydroponic culture. Dry weights of shoots and roots were not affected by salinity; however E. purpurea and E. pallida exhibited higher survival rate than E. angustifolia, which also showed high salt injury index and electrolyte leakage compared to the other two species. Gas exchange (photosynthetic rate, stomatal conductance, and transpiration rate) showed a decline with increasing salt concentrations in all species with a more pronounced reduction in E. angustifolia. E. purpurea was able to retain more Na+ in the roots than the other two species showing its capacity to regulate Na+ translocation to shoots (Na+ exclusion). Moreover, the activities of two major antioxidant enzymes; superoxide dismutase (SOD) and ascorbate peroxidase (APX) were increased by salinity in E purperea, while the activities were decreased in E. angustifolia. The characteristic phytochemical profiles of caffeic acid derivatives (CADs) and alkamides/ketones were obtained for the three species, and quantitative changes were determined. Cichoric acid, the major CAD in E. purpurea, was increased with salinity up to 75 mM NaCl. A relative increase in alkamides and CADs was recorded in E. angustifolia, while in E. pallida, the level of echinacoside and major ketones (22 and 24) decreased, suggesting that the medicinal value of this species was compromised by salt stress. First evidence of salt-induced changes in alkamides and ketones in Echinacea was demonstrated in this study. Activity of phenylalanine ammonia-lyase (PAL), the major enzyme involved in the biosynthesis of CADs, was increased only in the roots of E. purpurea, further reflecting the differences in salt tolerance between species. It can be concluded that Echinacea species exhibited a limited degree of salt tolerance; however, E. purpurea showed a higher tolerance than E. pallida and E. angustifolia. This tolerance was mainly attributed to the increase in Na+ exclusion capacity, antioxidant activities and PAL activity.
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Estudo dos efeitos farmacolÃgicos de (O-METIL)-N-2,6-Dihidroxi-benzoil Tiramina (Riparina III) de Aniba Riparia (NEES) mez (Lauraceae) em modelos comportamentais de ansiedade e depressÃo em camundongos / Study of Pharmacological Effects of (O-Methyl)-N-2,6-dihydroxy-benzoyl-tyramine (riparin III) from Aniba riparia (Nees) Mez (Lauraceae) on behavioral models of anxiety and depression in miceCarla Thiciane Vasconcelos de Melo 11 December 2006 (has links)
Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico / A riparina III, alcamida isolada do fruto verde de Aniba riparia, foi avaliada em modelos animais clÃssicos para screening de drogas com atividade em ansiedade, depressÃo, sedaÃÃo e convulsÃo, tais como, campo aberto, rota rod, labirinto em cruz elevado (LCE), placa perfurada, nado forÃado, suspensÃo da cauda, hipotermia induzida por apomorfina, tempo de sono induzido por pentobarbital e convulsÃo induzida por pentilenotetrazol. A riparina III foi administrada de forma aguda em todos os testes, nas doses de 25 e 50 mg/kg, atravÃs das vias oral e intraperitoneal. Os resultados mostraram que esta alcamida nÃo alterou a atividade locomotora, mas diminuiu o nÃmero de rearing e grooming, no teste do campo aberto, sugerindo um possÃvel efeito ansiolÃtico. No LCE e no teste da placa perfurada, a riparina III comprovou seu efeito ansiolÃtico, pois aumentou todos os parÃmetros analisados no LCE, como NEBA, PEBA, TPBA e PTBA, assim como o nÃmero de head dips na placa perfurada. Este efeito està possivelmente relacionado com o sistema gabaÃrgico jà que o flumazenil, antagonista dos receptores GABAA/BenzodiazepÃnico, reverteu o efeito ansiolÃtico da riparina III no LCE. A avaliaÃÃo sedativa/hipnÃtica da riparina III, no teste do tempo de sono induzido por pentobarbital, mostrou uma potencializaÃÃo do sono, que parece estar envolvido com processos farmacocinÃticos ou com mecanismos de regulaÃÃo do sono, jà que o efeito sedativo nÃo foi corroborado no campo aberto. No teste da convulsÃo induzida por pentilenotetrazol, a riparina III protegeu parcialmente os animais da convulsÃo, assim como prolongou o tempo de vida, e, em alguns casos, atà impediu a morte dos animais. Esse resultado sugere um efeito anticonvulsivante da riparina III, possivelmente relacionado com o sistema gabaÃrgico, visto que hà um envolvimento desta substÃncia com os receptores GABAA/BenzodiazepÃnico mostrado no LCE. A riparina III tambÃm parece apresentar um efeito antidepressivo, pois no teste do nado forÃado e suspensÃo da cauda, esta substÃncia diminuiu o tempo de imobilidade dos animais. Este efeito antidepressivo nÃo parece estar relacionado com o sistema noradrenÃrgico, jà que no teste da hipotermia induzida por apomorfina, a riparina III potencializou, ao invÃs de antagonizar, a hipotermia. O efeito de antagonizar a hipotermia à uma caracterÃstica de drogas antidepressivas do tipo imipramina, descartando assim, o envolvimento da riparina III com o sistema noradrenÃrgico. No entanto, o efeito antidepressivo da riparina III parece estar envolvido com o sistema dopaminÃrgico, pois, o antagonista dos receptores dopaminÃrgicos do tipo D2, sulpirida, reverteu o efeito da riparina III no nado forÃado. Por outro lado, o antagonista dopaminÃrgico do tipo D1, SCH23390, nÃo reverteu este efeito. Esse resultado sugere, entÃo, que o efeito antidepressivo desta alcamida, se dà pelo envolvimento com o sistema dopaminÃrgico, especificamente com os receptores do tipo D2. Em conclusÃo, esses efeitos mostraram que a riparina III apresenta efeito ansiolÃtico e anticonvulsivante, provavelmente relacionado com o sistema gabaÃrgico e efeito antidepressivo, provavelmente relacionado com o sistema dopaminÃrgico / Riparin III, an alkamide isolated from unripe fruit of Aniba riparia, was evaluated in animal classical models for screening of new drugs in anxiety, depression, sedation and convulsion, such as, open field, rota rod, plus maze, hole board, forced swimming, tail suspension, apomorphine-induced hypothermia, pentobarbital-induced sleeping time and pentilenotetrazole-induced seizures tests. Riparin III was administered acutely in all tests, at doses of 25 e 50 mg/kg, through oral and intraperitoneal routes. The results showed that this alkamide did not alter the locomotor activity, but decreased the number of rearing and grooming, in the open field test, suggesting a possible anxiolytic effect. In the plus maze and hole board tests, riparin III presented anxiolytic effect due to an increase in all parameters analyzed, such as, NEOA, PEOA, TPOA and PTOA, in the plus maze, and an increase in the number of head dips in the hole board test. This effect is possible related with GABAergic system, since flumazenil, an antagonist of GABAA/Benzodiazepinic receptors, reversed the anxiolytic effect of riparin III, in the plus maze test. The sedative/hypnotic evaluation of riparin III, in pentobarbital-induced sleeping time, showed a sleeping potentiation that seems to be involved with pharmacokinetic processes or sleeping regulation mechanisms, since the sedative effect of riparin III was not corroborated in the open field test. In the pentilenotetrazole-induced seizures test, riparin III partially protected the animals from seizures, increased the death time, and in some cases, even protected the animals from death. This result may suggest an anticonvulsant effect of riparin III, possible related to GABAergic system, since there is an involvement of this substance with GABAA/Benzodiazepinic receptor, seen in plus maze test. Riparin III also presents an antidepressant effect, since in the forced swimming and tail suspension tests, this substance decreased the immobility time of the animals. This antidepressant effect does not seem to be related with noradrenergic system, since in the apomorphine-induced hypothermia test, riparin III potentiated instead of antagonizing, the hypothermia. It is known that the hypothermia-antagonized effect is a characteristic of antidepressant drugs, such as imipramine-like drugs. This way, it can be eliminated the possible involvement of riparin III with noradrenergic system. On the other hand, the antidepressant effect of riparin III seems to be related with dopaminergic system, since the antagonist of D2 dopaminergic receptor, sulpiride, reverted riparin III effect in the forced swimming test. However, the antagonist of D1 dopaminergic receptor, SCH23390, did not revert this effect. This result suggests that the antidepressant effect of this alkamide is involved with dopaminergic system, specifically with D2 dopaminergic receptor. In conclusion, these efects showed that riparin III presents anxiolytic and anticonvulsant effects, probably related with GABAergic system, and presents antidepressant effect, probably related with dopaminergic system
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Estudo dos Efeitos Antinociceptivos e AntiinflamatÃrios de (O-Metil)-N-Benzoil Tiramina (Riparina I) de Aniba Riparia (Nees) Mez (Lauraceae) em Camundongos / Study of Antinociceptive and Antiantiinflamatory Effects of (O-Methyl)-N-benzoyl-tyramine (riparin I) from Aniba riparia (Nees) Mez (Lauraceae)in mice.Fernando Luiz Oliveira de AraÃjo 01 August 2007 (has links)
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / A riparina I, alcamida isolada do fruto verde de Aniba riparia, foi avaliada em modelos animais clÃssicos para screening de drogas com atividades antinociceptiva, antiinflamatÃria e antiulcerogÃnica, tais como, contorÃÃes abdominais induzidas por Ãcido acÃtico, teste da formalina, placa quente, edema de pata induzido por carragenina e dextrano, Ãlcera gÃstrica induzida por etanol e indometacina, edema de pata e nocicepÃÃo induzidos por glutamato, como tambÃm em modelos comportamentais que permitam excluir a possibilidade de uma atividade central induzir falsos-positivos nos modelos anteriores, tais como testes do campo aberto, rota rod e tempo de sono induzido por pentobarbital. A riparina I foi administrada de forma aguda em todos os testes, nas doses de 25 e 50 mg/kg, atravÃs das vias oral e intraperitoneal. Os resultados mostraram que esta alcamida nÃo alterou a atividade locomotora no teste do campo aberto, nem diminuiu o nÃmero de quedas no teste do rota rod, descartando a possibilidade de haver sedaÃÃo ou incoordenaÃÃo motora por parte de riparina I, de modo que tais parÃmetros gerassem falsos-positivos nos testes de nocicepÃÃo e inflamaÃÃo. A avaliaÃÃo sedativa/hipnÃtica da riparina I, no teste do tempo de sono induzido por pentobarbital, mostrou uma potencializaÃÃo do sono, que parece estar envolvido com processos farmacocinÃticos ou com mecanismos de regulaÃÃo do sono, jà que o efeito sedativo nÃo foi corroborado no campo aberto. No teste das contorÃÃes induzidas por Ãcido acÃtico, riparina I inibiu significativamente o nÃmero de contorÃÃes, sugerindo uma atividade antinociceptiva. Como este teste à inespecÃfico, jà que vÃrias classes de drogas revertem estas contorÃÃes, foram utilizados modelos mais especÃficos para avaliar a atividade antinociceptiva. No teste da formalina, riparina I inibiu significativamente o tempo de lambedura da pata, tanto na fase nociceptiva do teste, como na fase inflamatÃria. No entanto, o papel antinociceptivo de riparina I parece ser devido sua atividade antiinflamatÃria, jà que a naloxona, um antagonista opiÃide, nÃo foi capaz de reverter o efeito antinociceptivo de riparina I, porÃm, a L-arginina, substrato para o mediador inflamatÃrio Ãxido nÃtrico, foi capaz de reverter este efeito. Para melhor avaliar o papel antiinflamatÃrio de riparina I, utilizaram-se outros modelos mais especÃficos. No edema de pata induzido por carragenina, riparina I foi capaz de reverter significativamente o volume de edema, nos tempos estudados, sugerindo que possa estar inibindo a produÃÃo de histamina, bradicinina, serotonina e prostaglandinas, mediadores inflamatÃrios secretados durante o processo. Como a bradicinina à um mediador nociceptivo comum a primeira fase do teste da formalina e ao edema de carragenina, este resultado sugere uma razÃo para a reversÃo significativa no tempo de lambedura de pata na primeira fase do teste da formalina. Riparina I tambÃm foi capaz de reverter, de maneira significativa, o edema de pata induzido por dextrano, sugerindo que esteja inibindo a produÃÃo de histamina e serotonina, mediadores inflamatÃrios secretados no processo. Riparina I inibiu significativamente o percentual de Ãrea ulcerada tanto em Ãlceras induzidas por indometacina como por etanol, ressaltando sua utilidade como antiinflamatÃrio nÃo ulcerogÃnico. Por fim, riparina I tambÃm foi capaz de diminuir tanto a nocicepÃÃo quanto o volume do edema de pata induzidos por glutamato, sugerindo que possa estar atuando como antagonista dos receptores glutamatÃrgicos envolvidos no processo inflamatÃrio. Concluindo, riparina I parece apresentar propriedades antiinflamatÃrias pela inibiÃÃo de mediadores como histamina, serotonina, bradicinina, prostaglandinas, glutamato e Ãxido nÃtrico, descartando o envolvimento do sistema opiÃide neste processo. / Riparin I, an alkamide isolated from unripe fruit of Aniba riparia, was evaluated in animal classical models for screening of drugs with antinociceptive, antiinflammatory and antiulcerogenic effects. These models are acetic acid-induced writhing test, formalin test, hot plate test, carrageenan-induced paw oedema, dextran-induced paw oedema, glutamate-induced nociception and paw oedema, indomethacin- and ethanol-induced gastric ulcer. Some behavioral models were used to evaluate if a central activity of drug were involved in antiinflammatory and antinociceptive properties of riparin I. These models are open field, rota rod and pentobarbital-induced sleeping time. Riparin I was administered with doses of 25 and 50 mg/kg, orally and intraperitoneally. The results show that this alkamide did not have effects neither on open field test nor on the rota rod test, discarding the possibility of sedation or motor incordination have influence in antiinflammatory/antinociceptive effects of riparin I. The sedative/hypnotic evaluation in pentobarbital-induced sleeping time shows an increase in sleeping time, probably due pharmacokynetics or sleeping regulation mechanisms, because the sedative effect was not corroborated in the open field test. The open field test is considered more specific than pentobarbital-induced sleeping time. In acetic acid-induced writhing test, riparin I decrease the number of writhies, suggesting an antinociceptive effect. This test is a non-specific test, because antiinflammatory, antidepressant and opioid drugs can decrease the number of writhies. In formalin test, riparin I decrease pawÂs licking time in both phases of test, suggesting antinociceptive and antiinflammatory effects. The antinociceptive effect of riparin I seems to be due their antiinflamatory properties, since naloxone could not abolish the antinociceptive effect of riparin I, but, L-arginine could. In the carrageenan-induced paw oedema test, riparin I decrease this parameter, suggesting that riparin I acts inhibiting the syntesis of bradykinin, serotonin, hystamin and prostaglandins, mediators involved in this test. This result probably indicates why riparin I decrease the pawÂs licking time in first phase of formalin test, since bradykinin is a common mediator involved in first phase of formalin test and carrageenan-induced paw oedema test. In the dextran-induced paw oedema test, riparin I decrease this parameter, suggesting that riparin I acts inhibiting the syntesis of serotonin and hystamin, mediators involved in this test. Riparin I decreased the ulcerated area induced by indomethacin and ethanol, outstanding your properties like antiinflammatory drug, but not like an ulcerogenic drug. Riparin I could decrease the nociception and the paw oedema, both induced by glutamate, suggesting that riparin I can inhibit the glutamatergic receptors involved in inflammatory processes. In conclusion, riparin I seems act by inhibition of inflammatory mediators like hystamin, serotonin, bradykinin, prostaglandins, glutamate and nitric oxide and seems do not act by opioid system.
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