RESUMO
The aim of our study is to estimate the hepatoprotective effects of the ethanolic extract of the leaves of Sequoia sempervirens by determination of liver biomarkers (ALT, AST, total bilirubin and albumin in serum) and by histopathological examinations using thioacetamide-induced (TAA) liver injury model. Concurrent administration of ethanolic extracts of S. sempervirens leaves improved the alterations in liver morphology where it was a potent protector of the liver. The potential of L-phenylalanine and silver nitrate as chemical elicitors as well as UV radiation as a physical elicitor on flavonoid production in callus culture of S. sempervirens were emphasized. Murashige and Skoog's medium fortified with phenylalanine and silver nitrate enhanced the production of flavonoids and phenolics. HPLC analysis was performed for qualitative and quantitative estimation of some flavonoid compounds in the produced calli in comparison with the mother plant. This finding highlights the potential use of S. sempervirens in the treatment of liver dysfunction.
Assuntos
Flavonoides/farmacologia , Fígado/efeitos dos fármacos , Fenóis/farmacologia , Substâncias Protetoras/farmacologia , Sequoia/citologia , Técnicas de Cultura de Tecidos/métodos , Animais , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Cromatografia Líquida de Alta Pressão , Meios de Cultura/química , Meios de Cultura/farmacologia , Flavonoides/análise , Flavonoides/metabolismo , Fígado/metabolismo , Hepatopatias/tratamento farmacológico , Hepatopatias/prevenção & controle , Masculino , Camundongos , Fenóis/análise , Fenóis/metabolismo , Extratos Vegetais/química , Extratos Vegetais/farmacologia , Folhas de Planta/química , Folhas de Planta/citologia , Substâncias Protetoras/química , Ratos Wistar , Sequoia/efeitos dos fármacos , Sequoia/crescimento & desenvolvimento , Sequoia/metabolismo , Tioacetamida/toxicidadeRESUMO
OBJECTIVE: It is well known that i.m. glucagon administration stimulates GH and cortisol release in humans, although the mechanisms are unclear. These effects are similar to those described for ghrelin on somatotroph and corticotroph function. The aim of the present study was to investigate the role of ghrelin in mediating the stimulatory effects of glucagon and to evaluate the effect of glucagon on ghrelin secretion. DESIGN AND METHODS: We studied the endocrine and metabolic response to i.m. glucagon administration in 24 subjects (14 men, 10 women; age 19-65 years; body mass index, 25.3 +/- 1 kg/m(2)), who were shown to have an intact anterior pituitary function as evaluated before enclosure. RESULTS: Serum ghrelin concentrations fell significantly at 30, 60, 120 and 180 min after glucagon administration (means +/- s.e.m.; baseline, 377.9 +/- 34.5 pg/ml; nadir, 294.6 +/- 28.3 pg/ml (60 min); P < 0.01). Conversely, i.m. glucagon elicited an increase in GH (baseline, 1.5 +/- 0.4 microg/l; peak, 14.2 +/- 2.7 microg/l (180 min); P < 0.01) and cortisol concentrations (baseline, 452.6 +/- 35.2 nmol/l; peak, 622.1 +/- 44 nmol/l (180 min); P < 0.01). The changes in ghrelin concentration at both 120 and 180 min were still significant after correction for glucose and insulin (P < 0.05). CONCLUSIONS: We show that i.m. glucagon decreases ghrelin significantly. Therefore, the already known stimulatory effects of i.m. glucagon on cortisol and GH are not mediated by a change in ghrelin concentrations. The mechanisms underlying the ghrelin suppression after i.m. glucagon are unlikely to include glucose or insulin variations and need to be further elucidated.