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1.
Endocr Regul ; 53(4): 221-230, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31734652

RESUMO

OBJECTIVES: Acute pancreatitis (AP) is a life-threatening condition. Using antioxidants in AP is insufficient and conflicting. Therefore, this study compared the effect of hydrogen sulfide (H2S) donor, sodium hydrosulfide (NaHS), leptin or curcumin pretreatment on AP induced by L-arginine. METHODS: Forty adult male rats were used and classified into: 1) control; 2) AP group [each rat was intraperitoneally (i.p.) injected with 2 doses of L-arginine of 250 mg/100 g body weight (b.w.) with an interval of 1 h]; 3) NaHS+AP group (each rat was i.p. injected with 10 mg/kg b.w. of NaHS 1 h before induction of AP); 4) leptin+AP group (each rat was pretreated with 10 µg/kg b.w. of leptin 30 min before induction of AP; and 5) curcumin+AP group (in which rats were i.p. injected with 150 mg/kg b.w. of curcumin 30 min before induction of AP). Serum amylase, lipase, nitric oxide (NO), tumor necrosis factor alpha (TNF-α), and corticosterone (CORT) levels were assayed. In addition, pancreatic tissues were obtained for histopathological examination and malondialde-hyde (MDA), total antioxidant capacity (TAC), and inducible nitric oxide synthase (iNOS) levels were measured. RESULTS: All AP treated groups showed significant decrease in serum levels of pancreatic enzymes, NO, and TNF-α, and pancreatic MDA and iNOS levels, while TAC levels were significantly increased. NaHS caused more limitation of inflammation than leptin and curcumin by affecting iNOS. Leptin was more potent than curcumin due to the stimulatory effect of leptin on glucocorticoid release to counteract inflammation. CONCLUSIONS: NaHS was more effective in AP amelioration than the leptin and curcumin.


Assuntos
Curcumina/farmacologia , Citoproteção/efeitos dos fármacos , Leptina/farmacologia , Pâncreas/efeitos dos fármacos , Pancreatite/prevenção & controle , Sulfetos/farmacologia , Animais , Arginina , Corticosterona/fisiologia , Masculino , Óxido Nítrico Sintase Tipo II/fisiologia , Pâncreas/metabolismo , Pâncreas/patologia , Pancreatite/induzido quimicamente , Pancreatite/metabolismo , Substâncias Protetoras/farmacologia , Ratos , Ratos Wistar , Transdução de Sinais
2.
J Cell Physiol ; 234(6): 8426-8435, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30443939

RESUMO

Polycystic ovary syndrome (PCOS), one of the important endocrine disorders affecting females in the reproductive age, is caused mainly by an abnormal oxidation status that subsequently causes inflammatory conditions. Thus, this study aims to examine the possible individual prophylactic effects of gasotransmitters, hemin, or L-arginine in letrozole-induced PCOS. Fifty adult female albino rats were used and separated into a control group, which received the vehicle; a letrozole-induced PCOS group (L), which received letrozole orally at a dose level of 1 mg/kg for 21 days; a letrozole+hemin (L+H) group, which received letrozole plus hemin at a dose level of 25 mg/kg injected IP twice per week for 21 days; and a letrozole+L-arginine (L+A) group, which received letrozole plus L-arginine at a dose level of 200 mg/kg orally for 21 days. During PCO induction, the body weight and Lee index were measured. Serum glucose, insulin, lipid profile, gonadotrophic hormones, testosterone, estrogen, and tumor necrosis factor alpha were assayed, while ovarian tissues were analyzed to measure the oxidative state and histopathological changes. Our results proved that either hemin or L-arginine administration could improve the oxidative state, the inflammatory reaction, the hormonal imbalance, and the metabolic disturbances in PCO rats, which was confirmed by a histopathological examination of the rats' ovaries. In conclusion, either hemin or L-arginine had protective effects against PCOS with better pathophysiological changes with hemin.


Assuntos
Arginina/farmacologia , Hemina/farmacologia , Síndrome do Ovário Policístico/tratamento farmacológico , Animais , Inibidores da Aromatase/farmacologia , Peso Corporal/efeitos dos fármacos , Feminino , Gasotransmissores/farmacologia , Humanos , Letrozol/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Síndrome do Ovário Policístico/induzido quimicamente , Síndrome do Ovário Policístico/fisiopatologia , Ratos
3.
Biomed Pharmacother ; 108: 799-808, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30253372

RESUMO

Monosodium glutamate (MSG) is frequently consumed as a flavor enhancer or food additive. Possible MSG-induced injurious effects on some organs have been stated in experimental animal models. Thus, in this study we tried to clarify effect and possible mechanism of action of MSG on liver and kidney, and if this results affected by the addition of l-Arginine or vitamin D to it. Animals divided into; Control, MSG treated, MSG + vitamin D treated, MSG + L-arginine treated group. Serum separated to determine liver and kidney function parameters. Kidneys and livers dissected out for histological examination and for assay of oxidative stress markers. RESULTS: MSG increased body weight and produced liver and kidney dysfunctions. The MSG-induced oxidative liver and kidney damage was proved. Vitamin D and l- Arginine have been shown to protect and restore the liver and the kidney capabilities in MSG models injury via inhibiting oxidative damage, vitamin D or l- Arginine suppresses the increased food intake and body weight gain induced by MSG. CONCLUSIONS: due to injurious effect of MSG, it should be avoided especially in liver or kidney disorders, foods containing excess MSG can be fortified with vitamin D or l- Arginine to overcome its adverse effects.


Assuntos
Arginina/farmacologia , Nefropatias/tratamento farmacológico , Hepatopatias/tratamento farmacológico , Substâncias Protetoras/farmacologia , Glutamato de Sódio/efeitos adversos , Vitamina D/farmacologia , Animais , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Peso Corporal/efeitos dos fármacos , Aditivos Alimentares/efeitos adversos , Rim/efeitos dos fármacos , Rim/metabolismo , Nefropatias/induzido quimicamente , Nefropatias/metabolismo , Fígado/efeitos dos fármacos , Fígado/metabolismo , Hepatopatias/metabolismo , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley
4.
Gen Physiol Biophys ; 32(3): 421-8, 2013 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23846259

RESUMO

Renal ischemia-reperfusion (I/R) is the major cause of acute renal failure. Renal I/R have distant effects on other organs, especially the heart. The purpose of this study was to investigate cardiac lesion following bilateral renal ischemia (50 minutes) and reperfusion (48 hours) in adult rats, to test sex differences in the development of cardiac lesions after acute renal I/R and to investigate the effect of estrogen on this type of cardiac lesions. 70 adult albino rats were divided into 7 groups: control male, I/R male, control female, I/R female, female with bilateral ovariectomy, I/R female with bilateral ovariectomy and I/R female with bilateral ovariectomy treated with estrogen. Renal and cardiac functions in both sexes were deteriorated following acute renal I/R injury proved by the increase in serum urea, creatinine, lactate dehydrogenase and creatine kinase levels. These cardiac lesions are mainly due to the oxidative stress response in the form of the increase in cardiac tissue lipid peroxide, and the decrease in cardiac tissue glutathione reductase, superoxide dismutase and catalase levels. In conclusion, female rats are more protected from the renal and cardiac lesions following acute renal I/R injury than male, since estrogen significantly decreases these lesions mainly by inhibiting the oxidative stress response.


Assuntos
Cardiopatias/complicações , Cardiopatias/fisiopatologia , Isquemia/complicações , Rim/irrigação sanguínea , Traumatismo por Reperfusão/complicações , Caracteres Sexuais , Animais , Biomarcadores/metabolismo , Terapia de Reposição de Estrogênios , Estrogênios/metabolismo , Feminino , Cardiopatias/tratamento farmacológico , Cardiopatias/metabolismo , Masculino , Ovariectomia , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/tratamento farmacológico
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