Abstract:Background:Gentamicin (GM) nephrotoxicity accounts for 10–30% of the acute renal failure (ARF) among drug-induced ARF. In Ayurveda such side effects are considered as the poisonous effects of low potent poisons called gara viṣa. Bilvādi agada (BA), a classical formulation is indicated in gara viṣa and most of its ingredients have proven for their nephroprotective activity.Aim:The aim was to evaluate the effect of BA in GM-induced nephrotoxicity in male Wistar rats.Materials and Methods:BA, GM, normal saline we… Show more
“…Many plants have been used for the treatment of kidney failure in traditional system of medicine throughout the world (Kumar et al, 2013). Many research studies reported the protective effect of plant extracts on gentamicin induced nephrotoxocity, which supports our current studies (Kanna et al, 2015;Manimala et al, 2015;Padmalochana and Rajan, 2015;Shalaby and Hammouda, 2014;Tavafi et al, 2012). Tecoma stans leaves, bark and roots contain many biologically active chemicals and extracts from those tissues have been used in traditional folk medicine to treat many diseases and conditions (Liogier, 1990).…”
The present study was undertaken to evaluate the Ethanolic Extract of Tecoma stans (EETS) flowers for its protective effect on gentamicin-induced nephrotoxocity in rats. Nephrotoxocity was induced in rats by intraperitoneal administration of gentamicin 80 mg kgG 1 dayG 1 for seven days. Effect of concurrent administration of EETS at a dose of 500 mg kgG 1 dayG 1 given by intraperitoneal route was determined using serum and urinary creatinine and blood urea nitrogen as indicators of kidney damage. As nephrotoxocity of gentamicin is known to involve the induction of oxidative stress, so in vitro antioxidant activity, malondialdehyde (MDA) and glutathione (GSH) levels were also evaluated. Gentamicin-induced glomerular congestion and necrosis of kidney cells were found to be reduced in the group receiving EETS with gentamicin. Rats treated with gentamicin developed significant kidney dysfunction was observed from increased levels of urea, creatinine, sodium and decreased levels of protein, uric acid and potassium. In vitro studies revealed that the EETS posses significant antioxidant activity. The above results confirm that the flower extract acquire nephroprotective and regenerative capacity against gentamicin toxicity.
“…Many plants have been used for the treatment of kidney failure in traditional system of medicine throughout the world (Kumar et al, 2013). Many research studies reported the protective effect of plant extracts on gentamicin induced nephrotoxocity, which supports our current studies (Kanna et al, 2015;Manimala et al, 2015;Padmalochana and Rajan, 2015;Shalaby and Hammouda, 2014;Tavafi et al, 2012). Tecoma stans leaves, bark and roots contain many biologically active chemicals and extracts from those tissues have been used in traditional folk medicine to treat many diseases and conditions (Liogier, 1990).…”
The present study was undertaken to evaluate the Ethanolic Extract of Tecoma stans (EETS) flowers for its protective effect on gentamicin-induced nephrotoxocity in rats. Nephrotoxocity was induced in rats by intraperitoneal administration of gentamicin 80 mg kgG 1 dayG 1 for seven days. Effect of concurrent administration of EETS at a dose of 500 mg kgG 1 dayG 1 given by intraperitoneal route was determined using serum and urinary creatinine and blood urea nitrogen as indicators of kidney damage. As nephrotoxocity of gentamicin is known to involve the induction of oxidative stress, so in vitro antioxidant activity, malondialdehyde (MDA) and glutathione (GSH) levels were also evaluated. Gentamicin-induced glomerular congestion and necrosis of kidney cells were found to be reduced in the group receiving EETS with gentamicin. Rats treated with gentamicin developed significant kidney dysfunction was observed from increased levels of urea, creatinine, sodium and decreased levels of protein, uric acid and potassium. In vitro studies revealed that the EETS posses significant antioxidant activity. The above results confirm that the flower extract acquire nephroprotective and regenerative capacity against gentamicin toxicity.
“…frecuentemente en el tratamiento de infecciones producidas por bacterias aerobias gram negativas; sin embargo, su terapia está relacionada con una de las complicaciones más frecuentes, la nefrotoxicidad 1,2,3,4 . Las concentraciones elevadas de esta droga en la superficie del endotelio capilar glomerular y del epitelio tubular renal producen aumento de los niveles de creatinina sérica, alteraciones morfológicas como edema y necrosis a nivel tubular, todo esto produce un aumento del estrés oxidativo y toxicidad renal 2 .…”
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“…Las concentraciones elevadas de esta droga en la superficie del endotelio capilar glomerular y del epitelio tubular renal producen aumento de los niveles de creatinina sérica, alteraciones morfológicas como edema y necrosis a nivel tubular, todo esto produce un aumento del estrés oxidativo y toxicidad renal 2 . Estudios previos han demostrado que el efecto nefrotóxico de la gentamicina puede ser mediado por la sobreproducción de especies reactivas de oxigeno (EROS), y esto debido a un incremento significativo de hidroperóxidos lipídicos y radicales hidroxilos, lo que ocasiona lesión a nivel de las estructuras internas de la nefrona 3,4,5,6,7 .…”
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“…El Ácido ascórbico (AsA) o vitamina C es un potente antioxidante, soluble en agua, elimina de manera eficaz los radicales libres y EROS 8,9,10 . Además, la vitamina C interviene en muchos procesos metabólicos como la estimulación de la cicatrización, aumentando la síntesis de colágeno y hormonas 4 . Diversos estudios vienen demostrando las propiedades antimutagénicas, antigenotóxicas y anticlastogénicas del ácido ascórbico debido a su capacidad antioxidativa frente a la acción de los radicales libres 5,11 .…”
El objetivo del estudio fue determinar el efecto nefroprotector del extracto de camu camu en un modelo de nefrotoxicidad inducida por la gentamicina. Estudio de tipo experimental formado por 50 ratas Sprague Dawley que se dividieron aleatoriamente en cinco grupos de estudio: Al grupo control se le administró la solución salina, al grupo gentamicina se le indujo la nefrotoxicidad y a los grupos experimentales 1, 2 y 3 se les protegió con el extracto alcohólico de camu camu a diferentes dosis. La actividad nefroprotectora se evaluó por la cuantificación de la creatinina sérica, el peso y análisis histopatológico de los riñones. Los resultados evidenciaron una disminución significativa del nivel de creatinina en los grupos protegidos con el extracto alcohólico de camu camu con respecto al grupo gentamicina (p<0,05). Los grupos que recibieron camu camu presentaron un aumento gradual del peso de los riñones en una relación directa a la dosis del extracto (p<0,05). El análisis histológico evidenció pérdida epitelial, infiltrado inflamatorio intenso y congestión vascular en el grupo gentamicina, mientras que los grupos que recibieron camu camu con el extracto disminuyeron la gravedad del daño. Se concluye que el extracto de camu camu presentó una actividad nefroprotectora significativa en un modelo de nefrotoxicidad inducida por gentamicina.
“…[3] The mechanism of gentamicin-induced nephrotoxicity in rats is through generation of oxidative stress which is mainly due to the production of reactive oxygen species (ROS) such as superoxide anions, hydroxyl radicals, and hydrogen peroxide and inhibition of oxidative phosphorylation. [4,5] ROS may result in the development of oxidative stress that may cause kidney damage. [6] Various inflammatory mediators responsible for inflammation may also result…”
Introduction: Renal damage due to gentamicin is associated with oxidative stress. Gallic acid is a phenolic compound that possesses antioxidant and anti-inflammatory properties. Hence, an attempt was made to explore the nephroprotective activity of gallic acid in gentamicin-induced nephrotoxicity. Materials and Methods: Wistar albino rats of either sex were used. Experimental nephrotoxicity was produced by intraperitoneal administration of gentamicin for 8 days. Rats were divided into five groups: Group I-normal control (normal Saline), Group II-gentamicin only treated group (100 mg/kg), Group III-gentamicin (100 mg/kg) + Vitamin C (200 mg/kg), Group IV (treatment group)-gentamicin (100 mg/kg) + gallic acid (200 mg/kg), and Group V-gentamicin (100 mg/kg) + gallic acid (400 mg/kg). The period of drug administration was of 8 days, in which animals were treated with Vitamin C and gallic acid. After the treatment for 8 days, the animals were sacrificed for the investigation of biochemical parameters and histopathological examination. Results: Gentamicin-induced nephrotoxicity was successfully reproduced. Concurrent administration of gallic acid along with gentamicin significantly prevented the rise in level of serum creatinine, serum urea, blood urea nitrogen, and total protein. Administration of gallic acid also leads to increase glutathione and superoxide dismutase level in the kidney. Therefore, gallic acid had significantly prevented nephrotoxicity as compared to the group receiving gentamicin drug alone. Conclusion: These results showed that gallic acid is effective as nephroprotective agent.
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