ABSTRACT
The use of herbal remedies in various local communities throughout the world to assuage the scourge of indigenous diseases has gained tremendous popularity. One of the many plants species of herbal remedies is Moringa oleifera (horseradish) which has been widely used in West Africa and Nigeria in particular for treating numerous human ailments such as malnutrition, cardiovascular, hepatotocicity and many others. Regardless of its wide use by communities around the world, there is inadequate scientific information available on the actual pharmacological effects of ethanolic extract of Moringa oleifera leaves on the heart and kidney dysfunction. Hence this work aimed at determining the inhibitory activity of ethanolic extract of horseradish on oxidative stress in the heart and kidney of dexamethazone induced hypertensive wistar albino rats. The air-dried leaves of horseradish were pulverized and crude ethanolic extract was prepared. The animals were grouped into four groups of five animals each. Group A animals served as control and fed with water and feed while Groups B and C animals were administered with 0.5 mL of 40% w/v ethanolic extract of Moringa oleifera leaf and 0.5 ml of 1.67 mg/kg body weight dexamethasone respectively. Group D animals were treated with 0.5 ml of 1.67 mg/kg body weight dexamethasone and 0.5 mL of 40% ethanolic extract of Moringa oleifera leaf intermittently for 21 days. The results obtained from the study showed that the ethanolic extract of Moringa oleifera leaf possessed the ability to inhibit and reverse the dexamethasone mediated tissues oxidative damage of both organs as seen in cholesterol, reduced glutathione and malondialdehyde concentrations. The same protective trend was also observed in activities of alkaline phosphatase, aspartate transaminase, alanine transaminase and catalase enzymesin both organs of the hypertensive rats. Hence, ethanolic extract of Moringa oleifera leaf reduced the extent of antioxidant loss and restoration of organ dysfunction caused by dexamethasone in the rats.
ABSTRACT
Avaliou-se a inibição da produção do fator de necrose tumoral alfa (TNF-alfa) devido ao pré-tratamento com antiinflamatório esteroidal (dexametasona) e não esteroidal (diclofenaco sódico) em eqüinos com endotoxemia induzida experimentalmente. Foram utilizados 15 cavalos machos não castrados, distribuídos em três grupos de cinco animais: controle (C), diclofenaco sódico (DS) e dexametasona (DM). A endotoxemia subletal foi induzida pela infusão intravenosa (IV) de 0,1mg/kg/pv de lipopolissacarídeo (LPS) de Escherichia coli 055:B5, administrado em 250ml de solução estéril de cloreto de sódio a 0,9 por cento, durante 15min. Os cavalos do grupo-controle foram tratados com solução de cloreto de sódio a 9 por cento IV. Nos animais do grupo DS, administraram-se, por via oral, 2,2mg/kg de diclofenaco sódico e, nos do grupo DM, 1,1mg/kg de dexametasona IV, respectivamente, 60 e 30min antes da infusão da endotoxina. Mensurou-se, por meio de ensaio de toxicidade com células da linhagem L929, a concentração de TNF-alfa no soro e no líquido peritoneal às 0, 1», 3 e 6 horas após injeção do LPS. No grupo-controle, observou-se aumento significativo de TNF-alfa sérico, em relação ao valor basal e aos grupos DS e DM, 1,15 horas após a indução da endotoxemia. No líquido peritoneal, as concentrações observadas estavam abaixo daquelas da curva padrão de TNF-alfa, não havendo diferença entre os grupos (P>0,05)
The inhibition of tumor necrosis factor alpha (TNF-alpha) production due to pre-treatment with steroidal (dexamethazone) and non-steroidal (sodium diclofenac) anti-inflammatories was studied in horses under experimentally induced endotoxemy. Fifteen stallions were allotted into three groups of five animals each: control (C), sodium diclofenac (SD) and dexamethazone (DM). Sublethal endotoxemy was induced with 0.1mg/kg/bw Escherichia coli 055:B5 lipopolysaccharide (LPS), IV, administrated in 250ml of 0.9 percent sterile sodium chloride, during 15 minutes. Control group horses received 9 percent sodium chloride, IV. SD group animals were orally administrated 2.2mg/kg sodium diclofenac and DM horses received 1.1mg/kg dexamethazone, IV, 30 and 60 minutes before endotoxin infusion, respectively. TNF-alpha concentration was measured in serum and peritoneal fluid by toxicity assay using L929 lineage cells at 0, 1», 3 and 6 hours after LPS injection. Ninety minutes after endotoxemy induction, it was verified a significant increase of serum TNF-a concentration in horses from control group in relation to the basal values as well as results of horses from SD and DM groups. In peritoneal fluid, the measured concentrations were lower than those from TNF-a standard curve and difference among the groups was not verified (P>0.05)