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1.
Pakistan Journal of Pharmaceutical Sciences. 2009; 22 (4): 373-380
em Inglês | IMEMR | ID: emr-102257

RESUMO

Garlic contains many sulfhydryl compounds that act as antioxidants. However, the role of nitric oxide [NO] in inflammation is controversial. The aim of the present study is to investigate the possible protective effect of garlic against acetic acid-induced ulcerative colitis in rats, as well as the probable modulatory effect of L-arginine [NO precursor] on garlic activity. Intra-rectal inoculation of rats with 4% acetic acid for 3 consecutive days caused a significant increase in the colon weight and marked decrease in the colon length. In addition, acetic acid induced a significant increase in serum levels of nitrate as well as colonic tissue content of malondialdehyde [MDA]. Moreover, colonic tissue contents of glutathione [GSH], superoxide dismutase [SOD] and catalase [CAT] were markedly reduced. On the other hand, pre-treatment of rats with garlic [0.25g/kgbwt, orally] for 4 consecutive weeks and 3days during induction of colitis significantly reduced the increase in the colon weight induced by acetic acid and ameliorated alterations in oxidant and antioxidant parameters. Interestingly, oral co-administration of garlic [0.25g/kgbwt] and L-arginine [625mg/kgbwt] for the same period of garlic administration mitigated the changes in both colon weight and length induced by acetic acid and increased garlic effect on colon tissue contents of MDA and GSH. In conclusion, L-arginine can augment the protective effect of garlic against ulcerative colitis; an effect that might be mainly attributed to its NO donating property resulting in enhancement of garlic antioxidant effect. Further studies will be needed to determine which one of the active ingredients of garlic has the main antioxidant effect to be used with L-arginine


Assuntos
Humanos , Masculino , Animais de Laboratório , Animais , Alho/química , Colite Ulcerativa/tratamento farmacológico , Antioxidantes , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Ratos Wistar , Sinergismo Farmacológico , Ácido Acético , Superóxido Dismutase , Glutationa , Plantas Medicinais , Tamanho do Órgão/efeitos dos fármacos , Nitritos/sangue , Catalase
2.
Pakistan Journal of Pharmaceutical Sciences. 2009; 22 (2): 205-210
em Inglês | IMEMR | ID: emr-92350

RESUMO

Oxidative stress may play a key role in the pathogenesis of diabetic nephropathy. Propolis and its extract have antioxidant properties. The effect of ethanolic extract of propolis against experimental diabetes mellitus-associated changes was examined. Diabetes was induced experimentally in rats by i.p. injection of streptozotocin [STZ] in a dose of 60 mg/kg bwt for 3 successive days. Blood urea nitrogen [BNU], creatinine, glucose, lipid profile, malondialdehyde [MDA] and urinary albumin were measured. Superoxide dimutase [SOD], glutathione [GSH], catalase [CAT] and MDA were measured in the renal tissue. The results showed decreased body weight and increased kidney weight in diabetic animals. Compared to the control normal rats, diabetic rats had higher blood glucose, BNU, creatinine, total cholesterol, triglycerides, low-density lipoprotein-cholesterol [LDL-C], MDA and urinary albumin and lower high-density lipoprotein-cholesterol [HDL-C] levels. Moreover, renal tissue MDA was markedly increased while SOD, GSH and CAT were significantly decreased. Oral administration of propolis extract in doses of 100,200 and 300 mg/kg bwt improved the body and kidney weights, serum glucose, lipid profile, MDA and renal function tests. Renal GSH, SOD and CAT were significantly increased while MDA was markedly reduced. These results may suggest a strong antioxidant effect of propolis which can ameliorate oxidative stress and delay the occurrence of diabetic nephropathy in diabetes mellitus


Assuntos
Animais de Laboratório , Própole/administração & dosagem , Nefropatias Diabéticas/fisiopatologia , Nefropatias Diabéticas/prevenção & controle , Antioxidantes , Estreptozocina , Radicais Livres , Ratos Wistar , Estresse Oxidativo , Diabetes Mellitus Experimental
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