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Métodos Terapéuticos y Terapias MTCI
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1.
Environ Sci Pollut Res Int ; 27(20): 25082-25092, 2020 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-32342422

RESUMEN

Gastric ulcer is a worldwide disease. Helicobacter pylori is one of the most common chronic bacterial infections that induce chronic inflammation in the gastric mucosa, mediated by an array of pro-and inflammatory cytokines. The aim of this study was to investigate the possible therapeutic effects of Ginkgo biloba extract on gastric ulcer induced by ammonium hydroxide in rats and the potential underlying mechanisms. The study was done on 32 adult male Wistar albino rats, divided equally into 4 groups: normal control, gastric ulcer-induced group using 1 ml of 1% NH4OH orally, ulcer control group; rats received 1% carboxymethyl cellulose daily for 14 days after induction of ulcer and treated rats received orally 200 mg/kg Ginkgo biloba once daily for 14 days after induction of ulcer. The study revealed administration of ammonia showed multiple gastric lesions; edema, hyperemia, hemorrhage, and ulcers with a significant increase in ulcer score, myeloperoxidase (MPO), and interleukin-1ß (IL-1ß) and a significant decrease in reduced glutathione (GSH), mucus amount, and gastric pH. After the administration of Ginkgo biloba, there was an improvement in gastric lesions, with a significant reduction of ulcer score, MPO, and IL-1ß and a significant increase in GSH, mucus content, and gastric pH. Moreover, collagen types I and IV were gradually increased in the treated group.


Asunto(s)
Úlcera Gástrica , Amoníaco , Animales , Ginkgo biloba , Masculino , Extractos Vegetales , Ratas , Ratas Wistar
2.
Pharmacol Res ; 53(4): 324-30, 2006 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-16458529

RESUMEN

Intestinal inflammatory states, regardless of specific initiating events, share common immunologically mediated pathways of tissue injury and repair. The efficacy of various drugs used to treat ulcerative colitis (UC) was investigated. The aim of the present study is to evaluate the effects of ginkgo biloba extract on the extent and severity of UC caused by intracolonic administration of acetic acid in rats. The inflammatory response was assessed by histology and measurement of myeloperoxidase activity (MPO), reduced glutathione (GSH), tumor necrosis factor (TNF-alpha) and interleukin-1beta (IL-1beta) levels in colon mucosa. Oral pretreatment with Ginkgo biloba in doses of (30, 60, 120 mg kg(-1) body weight) and sulfasalazine in a dose of (500 mg kg(-1) body weight used as reference) for 2 days before induction of colitis and continued for 5 consecutive days, significantly decreased colonic MPO activity, TNF-alpha, and IL-1beta levels and increased GSH concentration. Moreover, Ginkgo biloba attenuated the macroscopic colonic damage and the histopathological changes-induced by acetic acid. These results suggest that Ginkgo biloba may be effective in the treatment of UC through its scavenging effect on oxygen-derived free radicals.


Asunto(s)
Colitis Ulcerosa/tratamiento farmacológico , Colitis Ulcerosa/inmunología , Ginkgo biloba , Mucosa Intestinal/efectos de los fármacos , Mucosa Intestinal/inmunología , Extractos Vegetales/farmacología , Ácido Acético , Animales , Colitis Ulcerosa/inducido químicamente , Colitis Ulcerosa/metabolismo , Modelos Animales de Enfermedad , Glutatión/metabolismo , Interleucina-1/metabolismo , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patología , Masculino , Peroxidasa/metabolismo , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa/metabolismo
3.
Toxicol Appl Pharmacol ; 205(1): 43-52, 2005 May 15.
Artículo en Inglés | MEDLINE | ID: mdl-15885263

RESUMEN

Ulcerative colitis is a common inflammatory bowel disease (IBD) of unknown etiology. Recent studies have revealed the role of some microorganisms in the initiation and perpetuation of IBD. The role of antibiotics in the possible modulation of colon inflammation is still uncertain. In this study, we evaluated the effects of two macrolides, namely azithromycin and erythromycin, at different doses on the extent and severity of ulcerative colitis caused by intracolonic administration of 3% acetic acid in rats. The lesions and the inflammatory response were assessed by histology and measurement of myeloperoxidase (MPO) activity, nitric oxide synthetase (NOS) and tumor necrosis factor alpha (TNFalpha) in colonic tissues. Inflammation following acetic acid instillation was characterized by oedema, diffuse inflammatory cell infiltration and necrosis. Increase in MPO, NOS and TNFalpha was detected in the colonic tissues. Administration of either azithromycin or erythromycin at different dosage (10, 20 and 40 mg/kg orally, daily for 5 consecutive days) significantly (P < 0.05) reduced the colonic damage, MPO and NOS activities as well as TNFalpha level. This reduction was highly significant with azithromycin when given at a dose of 40 mg/kg. It is concluded that azithromycin and erythromycin may have a beneficial therapeutic role in ulcerative colitis.


Asunto(s)
Azitromicina/uso terapéutico , Colitis Ulcerosa/tratamiento farmacológico , Eritromicina/uso terapéutico , Ácido Acético/administración & dosificación , Ácido Acético/efectos adversos , Animales , Azitromicina/administración & dosificación , Azitromicina/metabolismo , Colitis Ulcerosa/inducido químicamente , Colitis Ulcerosa/metabolismo , Colon/efectos de los fármacos , Colon/enzimología , Colon/fisiopatología , Modelos Animales de Enfermedad , Relación Dosis-Respuesta a Droga , Evaluación Preclínica de Medicamentos/métodos , Eritromicina/administración & dosificación , Eritromicina/metabolismo , Interferón gamma/antagonistas & inhibidores , Interferón gamma/efectos de los fármacos , Interferón gamma/metabolismo , Masculino , Óxido Nítrico Sintasa/antagonistas & inhibidores , Óxido Nítrico Sintasa/efectos de los fármacos , Óxido Nítrico Sintasa/metabolismo , Peroxidasa/antagonistas & inhibidores , Peroxidasa/química , Peroxidasa/metabolismo , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/química , Factor de Necrosis Tumoral alfa/metabolismo
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