RESUMEN
PURPOSE: To examine effects of resveratrol on renal ischemia/ reperfusion injury (I/R) in a streptozotocin (STZ)-induced diabetic rat model. METHODS: Twenty-four male Sprague Dawley rats were treated with STZ injection for the development of diabetes, and divided into the following groups: Sham group, I/R group and Resveratrol group (n=8). Resveratrol (RSV) was administered at a dose of 10 mg.kg-1.d-1 fourteen days prior to suffering from I/R. Renal function, histology, SOD, MDA, TUNEL assay and expression of TNF-α, IL-1ß, NF-κB-P65, COX-2 and Caspase3, Bcl2 and Bax were analyzed. RESULTS: Administration of RSV significantly reduced the serum levels of renal dysfunction and injury markers, including creatinine, blood urea nitrogen and MDA; in the other hand, it significantly increased the serum levels of SOD. The protective effect of RSV was also reflected on histologic evaluation. RSV reduced the number of apoptotic cells as determined by TUNEL assay. RSV significantly reduced the protein expression of TNF-α, IL-1ß, NF-κB-P65, COX-2 and Caspase3, and Bax. Meanwhile, RSV significantly increased the protein expression of Bcl2. CONCLUSION: RSV attenuated I/R-induced renal injury in diabetic rats through the modulation of oxidative stress and TNF-α-stimulated inflammation.
Asunto(s)
Antioxidantes , Diabetes Mellitus Experimental , Daño por Reperfusión , Resveratrol , Animales , Antioxidantes/farmacología , Inflamación , Riñón , Masculino , Ratas , Ratas Sprague-Dawley , Daño por Reperfusión/prevención & control , Resveratrol/farmacología , Factor de Necrosis Tumoral alfaRESUMEN
Purpose To examine effects of resveratrol on renal ischemia/ reperfusion injury (I/R) in a streptozotocin (STZ)-induced diabetic rat model. Methods Twenty-four male Sprague Dawley rats were treated with STZ injection for the development of diabetes, and divided into the following groups: Sham group, I/R group and Resveratrol group (n=8). Resveratrol (RSV) was administered at a dose of 10 mg.kg-1.d-1 fourteen days prior to suffering from I/R. Renal function, histology, SOD, MDA, TUNEL assay and expression of TNF-alfa, IL-1beta, NF-kB-P65, COX-2 and Caspase3, Bcl2 and Bax were analyzed. Results Administration of RSV significantly reduced the serum levels of renal dysfunction and injury markers, including creatinine, blood urea nitrogen and MDA; in the other hand, it significantly increased the serum levels of SOD. The protective effect of RSV was also reflected on histologic evaluation. RSV reduced the number of apoptotic cells as determined by TUNEL assay. RSV significantly reduced the protein expression of TNF-alfa, IL-1beta, NF-B-P65, COX-2 and Caspase3, and Bax. Meanwhile, RSV significantly increased the protein expression of Bcl2. Conclusion RSV attenuated I/R-induced renal injury in diabetic rats through the modulation of oxidative stress and TNF-alfa-stimulated inflammation.(AU)
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Animales , Ratas , Isquemia/veterinaria , Reperfusión/veterinaria , Resveratrol/uso terapéutico , Inflamación/tratamiento farmacológico , Inflamación/veterinaria , Ratas Sprague-Dawley , Diabetes Mellitus/veterinariaRESUMEN
Abstract Purpose To examine effects of resveratrol on renal ischemia/ reperfusion injury (I/R) in a streptozotocin (STZ)-induced diabetic rat model. Methods Twenty-four male Sprague Dawley rats were treated with STZ injection for the development of diabetes, and divided into the following groups: Sham group, I/R group and Resveratrol group (n=8). Resveratrol (RSV) was administered at a dose of 10 mg.kg-1.d-1 fourteen days prior to suffering from I/R. Renal function, histology, SOD, MDA, TUNEL assay and expression of TNF-α, IL-1β, NF-κB-P65, COX-2 and Caspase3, Bcl2 and Bax were analyzed. Results Administration of RSV significantly reduced the serum levels of renal dysfunction and injury markers, including creatinine, blood urea nitrogen and MDA; in the other hand, it significantly increased the serum levels of SOD. The protective effect of RSV was also reflected on histologic evaluation. RSV reduced the number of apoptotic cells as determined by TUNEL assay. RSV significantly reduced the protein expression of TNF-α, IL-1β, NF-κB-P65, COX-2 and Caspase3, and Bax. Meanwhile, RSV significantly increased the protein expression of Bcl2. Conclusion RSV attenuated I/R-induced renal injury in diabetic rats through the modulation of oxidative stress and TNF-α-stimulated inflammation.
Asunto(s)
Animales , Masculino , Ratas , Daño por Reperfusión/prevención & control , Diabetes Mellitus Experimental , Resveratrol/farmacología , Antioxidantes/farmacología , Factor de Necrosis Tumoral alfa , Ratas Sprague-Dawley , Inflamación , RiñónRESUMEN
PURPOSE: To investigate the effect of Picroside II on testicular ischemia and reperfusion (l/R) injury and the underlying mechanism. METHODS: Sprague-Dawley rats were randomly divided into 4 groups: sham operated group (Sham), Sham with Picroside II treatment group (Sham+ Pic II), l/R group (l/R) and l/R with Picroside II treatment group (I/R+ Pic II). l/R model was established by rotating the left testis 720° in a clock-wise direction for 4 hours. The histopathologic and spermatogenetic evaluation was performed. The apoptosis changes and the levels of HO-1 (heme oxygenase-1), MPO (myeloperoxidase), NOX (NADPH oxidase), SOD (superoxide dismutase), XO (xanthine oxidase) and NOS (nitric oxide synthase) were measured. RESULTS: The seminiferous tubules were damaged in l/R rats, but Picroside II alleviated the changes induced by l/R. The increased level of apoptosis was decreased by Picroside II (P=0.01, 9.05±0.35 vs. 4.85±0.25). The activities of HO-1, MPO, NOX, XO and MDA content were increased and the SOD activity was decreased in l/R (P<0.05) and could be reversed by Picroside II (P=0.03, 405.5±7.5 vs. 304±17U/mgprot; P=0.02, 0.99±0.05 vs. 0.52±0.04 mgprot; P=0.01, 260+7 vs. 189±2 mgprot; P=0.04, 10.95+0.55 vs. 8.75+0.35 U/mgprot; P=0.045, 6.8+0.7 vs. 3.75+0.35 mgprot; P=0.04, 44.5+3.5 vs. 57.5+3.5 mgprot). Western blot showed that the expression of iNOS, nNOS and eNOS were increased in l/R (P<0.05); however, they were decreased after Picroside II treatment (P<0.05). CONCLUSION: Picroside II attenuated testicular I/R injury in rats mainly through suppressing apoptosis and oxidative stress through reduction of nitric oxide synthesis.
Asunto(s)
Apoptosis/efectos de los fármacos , Cinamatos/farmacología , Glucósidos Iridoides/farmacología , Óxido Nítrico/biosíntesis , Estrés Oxidativo/efectos de los fármacos , Daño por Reperfusión/prevención & control , Testículo/irrigación sanguínea , Animales , Western Blotting , Hemo-Oxigenasa 1/análisis , Etiquetado Corte-Fin in Situ , Masculino , Malondialdehído/análisis , NADP/análisis , Peroxidasa/análisis , Distribución Aleatoria , Ratas Sprague-Dawley , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Reproducibilidad de los Resultados , Superóxido Dismutasa/análisis , Testículo/patología , Xantina Oxidasa/análisisRESUMEN
Abstract Purpose: To investigate the effect of Picroside II on testicular ischemia and reperfusion (l/R) injury and the underlying mechanism. Methods: Sprague-Dawley rats were randomly divided into 4 groups: sham operated group (Sham), Sham with Picroside II treatment group (Sham+ Pic II), l/R group (l/R) and l/R with Picroside II treatment group (I/R+ Pic II). l/R model was established by rotating the left testis 720° in a clock-wise direction for 4 hours. The histopathologic and spermatogenetic evaluation was performed. The apoptosis changes and the levels of HO-1 (heme oxygenase-1), MPO (myeloperoxidase), NOX (NADPH oxidase), SOD (superoxide dismutase), XO (xanthine oxidase) and NOS (nitric oxide synthase) were measured. Results: The seminiferous tubules were damaged in l/R rats, but Picroside II alleviated the changes induced by l/R. The increased level of apoptosis was decreased by Picroside II (P=0.01, 9.05±0.35 vs. 4.85±0.25). The activities of HO-1, MPO, NOX, XO and MDA content were increased and the SOD activity was decreased in l/R (P<0.05) and could be reversed by Picroside II (P=0.03, 405.5±7.5 vs. 304±17U/mgprot; P=0.02, 0.99±0.05 vs. 0.52±0.04 mgprot; P=0.01, 260+7 vs. 189±2 mgprot; P=0.04, 10.95+0.55 vs. 8.75+0.35 U/mgprot; P=0.045, 6.8+0.7 vs. 3.75+0.35 mgprot; P=0.04, 44.5+3.5 vs. 57.5+3.5 mgprot). Western blot showed that the expression of iNOS, nNOS and eNOS were increased in l/R (P<0.05); however, they were decreased after Picroside II treatment (P<0.05). Conclusion: Picroside II attenuated testicular I/R injury in rats mainly through suppressing apoptosis and oxidative stress through reduction of nitric oxide synthesis.
Asunto(s)
Animales , Masculino , Testículo/irrigación sanguínea , Daño por Reperfusión/prevención & control , Cinamatos/farmacología , Apoptosis/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Glucósidos Iridoides/farmacología , Óxido Nítrico/biosíntesis , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Distribución Aleatoria , Western Blotting , Ratas Sprague-Dawley , Peroxidasa/análisis , Etiquetado Corte-Fin in Situ , Hemo-Oxigenasa 1/análisis , Malondialdehído/análisis , NADP/análisisRESUMEN
Purpose: To investigate the effect of Picroside II on testicular ischemia and reperfusion (l/R) injury and the underlying mechanism. Methods: Sprague-Dawley rats were randomly divided into 4 groups: sham operated group (Sham), Sham with Picroside II treatment group (Sham+ Pic II), l/R group (l/R) and l/R with Picroside II treatment group (I/R+ Pic II). l/R model was established by rotating the left testis 720° in a clock-wise direction for 4 hours. The histopathologic and spermatogenetic evaluation was performed. The apoptosis changes and the levels of HO-1 (heme oxygenase-1), MPO (myeloperoxidase), NOX (NADPH oxidase), SOD (superoxide dismutase), XO (xanthine oxidase) and NOS (nitric oxide synthase) were measured. Results: The seminiferous tubules were damaged in l/R rats, but Picroside II alleviated the changes induced by l/R. The increased level of apoptosis was decreased by Picroside II (P=0.01, 9.05±0.35 vs. 4.85±0.25). The activities of HO-1, MPO, NOX, XO and MDA content were increased and the SOD activity was decreased in l/R (P 0.05) and could be reversed by Picroside II (P=0.03, 405.5±7.5 vs. 304±17U/mgprot; P=0.02, 0.99±0.05 vs. 0.52±0.04 mgprot; P=0.01, 260+7 vs. 189±2 mgprot; P=0.04, 10.95+0.55 vs. 8.75+0.35 U/mgprot; P=0.045, 6.8+0.7 vs. 3.75+0.35 mgprot; P=0.04, 44.5+3.5 vs. 57.5+3.5 mgprot). Western blot showed that the expression of iNOS, nNOS and eNOS were increased in l/R (P 0.05); however, they were decreased after Picroside II treatment (P 0.05). Conclusion: Picroside II attenuated testicular I/R injury in rats mainly through suppressing apoptosis and oxidative stress through reduction of nitric oxide synthesis.(AU)
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Animales , Ratas , Enfermedades Testiculares/terapia , Isquemia/terapia , Estrés Oxidativo , Óxido Nítrico/síntesis química , Ratas/lesionesRESUMEN
Glycogen storage disease type I and glycogenic hepatopathy are the most common type of primary and secondary hepatic glycogenosis, with presenting common radiological features of hepatomegaly, hepatic signal, or density change. Beyond that, glycogen storage disease type I shows hepatocellular adenomas or fatty liver, while glycogenic hepatopathy does not.
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Enfermedad del Almacenamiento de Glucógeno Tipo I/diagnóstico por imagen , Glucógeno/metabolismo , Hepatopatías/diagnóstico por imagen , Hígado/diagnóstico por imagen , Imagen por Resonancia Magnética , Tomografía Computarizada por Rayos X , Diagnóstico Diferencial , Enfermedad del Almacenamiento de Glucógeno Tipo I/metabolismo , Humanos , Hígado/metabolismo , Hepatopatías/metabolismo , Valor Predictivo de las PruebasRESUMEN
OBJECTIVE: Evaluate the efficiency and safety of bipolar plasma vaporization using plasma-cutting and plasma-loop electrodes for the treatment of posterior urethral stricture. Compare the outcomes following bipolar plasma vaporization with conventional cold-knife urethrotomy. METHODS: A randomized trial was performed to compare patient outcomes from the bipolar and cold-knife groups. All patients were assessed at 6 and 12 months postoperatively via urethrography and uroflowmetry. At the end of the first postoperative year, ureteroscopy was performed to evaluate the efficacy of the procedure. The mean follow-up time was 13.9 months (range: 12 to 21 months). If re-stenosis was not identified by both urethrography and ureteroscopy, the procedure was considered "successful". RESULTS: Fifty-three male patients with posterior urethral strictures were selected and randomly divided into two groups: bipolar group (n=27) or cold-knife group (n=26). Patients in the bipolar group experienced a shorter operative time compared to the cold-knife group (23.45±7.64 hours vs 33.45±5.45 hours, respectively). The 12-month postoperative Qmax was faster in the bipolar group than in the cold-knife group (15.54±2.78 ml/sec vs 18.25±2.12 ml/sec, respectively). In the bipolar group, the recurrence-free rate was 81.5% at a mean follow-up time of 13.9 months. In the cold-knife group, the recurrence-free rate was 53.8%. CONCLUSIONS: The application of bipolar plasma-cutting and plasma-loop electrodes for the management of urethral stricture disease is a safe and reliable method that minimizes the morbidity of urethral stricture resection. The advantages include a lower recurrence rate and shorter operative time compared to the cold-knife technique.
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Ablación por Catéter/métodos , Cistoscopía/métodos , Estrechez Uretral/cirugía , Anciano , Electrodos , Estudios de Seguimiento , Humanos , Tiempo de Internación/estadística & datos numéricos , Masculino , Persona de Mediana Edad , Tempo Operativo , Periodo Perioperatorio , Estudios Prospectivos , Recurrencia , Resultado del TratamientoRESUMEN
OBJECTIVE: Evaluate the efficiency and safety of bipolar plasma vaporization using plasma-cutting and plasma-loop electrodes for the treatment of posterior urethral stricture. Compare the outcomes following bipolar plasma vaporization with conventional cold-knife urethrotomy. METHODS: A randomized trial was performed to compare patient outcomes from the bipolar and cold-knife groups. All patients were assessed at 6 and 12 months postoperatively via urethrography and uroflowmetry. At the end of the first postoperative year, ureteroscopy was performed to evaluate the efficacy of the procedure. The mean follow-up time was 13.9 months (range: 12 to 21 months). If re-stenosis was not identified by both urethrography and ureteroscopy, the procedure was considered “successful”. RESULTS: Fifty-three male patients with posterior urethral strictures were selected and randomly divided into two groups: bipolar group (n=27) or cold-knife group (n=26). Patients in the bipolar group experienced a shorter operative time compared to the cold-knife group (23.45±7.64 hours vs 33.45±5.45 hours, respectively). The 12-month postoperative Qmax was faster in the bipolar group than in the cold-knife group (15.54±2.78 ml/sec vs 18.25±2.12 ml/sec, respectively). In the bipolar group, the recurrence-free rate was 81.5% at a mean follow-up time of 13.9 months. In the cold-knife group, the recurrence-free rate was 53.8%. CONCLUSIONS: The application of bipolar plasma-cutting and plasma-loop electrodes for the management of urethral stricture disease is a safe and reliable method that minimizes the morbidity of urethral stricture resection. The advantages include a lower recurrence rate and shorter operative time compared to the cold-knife technique.
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Anciano , Humanos , Masculino , Persona de Mediana Edad , Ablación por Catéter/métodos , Cistoscopía/métodos , Estrechez Uretral/cirugía , Electrodos , Estudios de Seguimiento , Tiempo de Internación/estadística & datos numéricos , Tempo Operativo , Periodo Perioperatorio , Estudios Prospectivos , Recurrencia , Resultado del TratamientoRESUMEN
PURPOSE: To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats. METHODS: Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected. RESULTS: Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels. CONCLUSION: Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.
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Apoptosis/efectos de los fármacos , Células Epiteliales/efectos de los fármacos , Precondicionamiento Isquémico/métodos , Riñón/irrigación sanguínea , Riñón/efectos de los fármacos , Metformina/farmacología , Daño por Reperfusión/prevención & control , Proteínas Quinasas Activadas por AMP/análisis , Animales , Nitrógeno de la Urea Sanguínea , Western Blotting , Caspasa 3/análisis , Creatinina/sangre , Ciclooxigenasa 2/análisis , Inmunohistoquímica , Riñón/patología , Masculino , Distribución Aleatoria , Ratas Sprague-Dawley , Reproducibilidad de los Resultados , Factores de TiempoRESUMEN
PURPOSE:To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats.METHODS:Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected.RESULTS:Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels.CONCLUSION:Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.
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Animales , Masculino , Apoptosis/efectos de los fármacos , Células Epiteliales/efectos de los fármacos , Precondicionamiento Isquémico/métodos , Riñón/irrigación sanguínea , Riñón/efectos de los fármacos , Metformina/farmacología , Daño por Reperfusión/prevención & control , Proteínas Quinasas Activadas por AMP/análisis , Nitrógeno de la Urea Sanguínea , Western Blotting , /análisis , Creatinina/sangre , /análisis , Inmunohistoquímica , Riñón/patología , Distribución Aleatoria , Ratas Sprague-Dawley , Reproducibilidad de los Resultados , Factores de TiempoRESUMEN
To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats. Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected. Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels. Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.(AU)
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Animales , Masculino , Apoptosis , Células Epiteliales , Precondicionamiento Isquémico/métodos , Riñón/irrigación sanguínea , Riñón , Metformina/farmacología , Daño por Reperfusión/prevención & control , Proteínas Quinasas Activadas por AMP/análisis , Nitrógeno de la Urea Sanguínea , Western Blotting , Caspasa 3/análisis , Creatinina/sangre , Ciclooxigenasa 2/análisis , Inmunohistoquímica , Riñón/patología , Distribución Aleatoria , Ratas Sprague-Dawley , Reproducibilidad de los Resultados , Factores de TiempoRESUMEN
PURPOSE: To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway. METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed. RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins. CONCLUSION: Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway.
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Alcaloides/farmacología , Antioxidantes/farmacología , Hemo-Oxigenasa 1/metabolismo , Riñón/irrigación sanguínea , Factor 2 Relacionado con NF-E2/metabolismo , Estrés Oxidativo/efectos de los fármacos , Quinolizinas/farmacología , Daño por Reperfusión/prevención & control , Alcaloides/uso terapéutico , Animales , Antioxidantes/uso terapéutico , Apoptosis/efectos de los fármacos , Western Blotting , Modelos Animales de Enfermedad , Hemo-Oxigenasa 1/análisis , Inmunohistoquímica , Etiquetado Corte-Fin in Situ , Riñón/patología , Masculino , Factor 2 Relacionado con NF-E2/análisis , Quinolizinas/uso terapéutico , Distribución Aleatoria , Ratas Sprague-Dawley , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Reproducibilidad de los Resultados , Factores de Tiempo , Resultado del TratamientoRESUMEN
PURPOSE: To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway. METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed. RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins. CONCLUSION: Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway. .
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Animales , Masculino , Alcaloides/farmacología , Antioxidantes/farmacología , Hemo-Oxigenasa 1/metabolismo , Riñón/irrigación sanguínea , /metabolismo , Estrés Oxidativo/efectos de los fármacos , Quinolizinas/farmacología , Daño por Reperfusión/prevención & control , Alcaloides/uso terapéutico , Antioxidantes/uso terapéutico , Apoptosis/efectos de los fármacos , Western Blotting , Modelos Animales de Enfermedad , Hemo-Oxigenasa 1/análisis , Inmunohistoquímica , Etiquetado Corte-Fin in Situ , Riñón/patología , /análisis , Quinolizinas/uso terapéutico , Distribución Aleatoria , Ratas Sprague-Dawley , Reproducibilidad de los Resultados , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Factores de Tiempo , Resultado del TratamientoRESUMEN
PURPOSE:To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway.METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed.RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins.CONCLUSION:Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway.(AU)
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Animales , Ratas , Extractos Vegetales/uso terapéutico , Sophora/química , Insuficiencia Renal/tratamiento farmacológico , Estrés Oxidativo , Daño por Reperfusión , Nefrectomía/veterinariaRESUMEN
PURPOSE: To investigate the protective effects of ozone oxidative preconditioning (OzoneOP) were associated with the modulation of TLR4-NF-κB pathway. METHODS: Thirty six rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated and immunohistochemistry was also performed for localization of TLR4 and NF-κB. The expression of TNF-α, IL-1ß, IL-6, ICAM-1 and MCP-1 were studied by Real-time PCR. Western blot was performed to detect the expression of TLR4 and NF-κB. RESULTS: The results indicated that blood urea nitrogen and creatinine levels increased significantly in I/R group. Rats treated with OzoneOP showed obviously less renal damage. Immunohistochemistry showed that TLR4 were ameliorated by OzoneOP. Realtime PCR showed that OzoneOP could significantly inhibit the increased mRNA levels of TNF-α, IL-1ß, IL-6, ICAM-1 and MCP-1 induced by I/R. Western blot indicated that the expression of TLR4 and NF-κB were upregulated in I/R group, but OzoneOP could inhibit this increase. CONCLUSION: These findings indicated that OzoneOP had potent anti-inflammatory properties by the modulation of the TLR4-NF-κB pathway in renal ischemia/reperfusion injury.
Asunto(s)
Precondicionamiento Isquémico/métodos , Riñón/irrigación sanguínea , FN-kappa B/análisis , Ozono/farmacología , Daño por Reperfusión/prevención & control , Receptor Toll-Like 4/análisis , Animales , Nitrógeno de la Urea Sanguínea , Western Blotting , Creatinina/sangre , Citocinas/análisis , Inmunohistoquímica , Molécula 1 de Adhesión Intercelular/análisis , Riñón/metabolismo , Masculino , FN-kappa B/metabolismo , Ratas Wistar , Reacción en Cadena en Tiempo Real de la Polimerasa , Reproducibilidad de los Resultados , Factores de Tiempo , Receptor Toll-Like 4/metabolismoRESUMEN
PURPOSE: To investigate the protective effects of ozone oxidative preconditioning (OzoneOP) were associated with the modulation of TLR4-NF-κB pathway. METHODS: Thirty six rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated and immunohistochemistry was also performed for localization of TLR4 and NF-κB. The expression of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 were studied by Real-time PCR. Western blot was performed to detect the expression of TLR4 and NF-κB. RESULTS: The results indicated that blood urea nitrogen and creatinine levels increased significantly in I/R group. Rats treated with OzoneOP showed obviously less renal damage. Immunohistochemistry showed that TLR4 were ameliorated by OzoneOP. Realtime PCR showed that OzoneOP could significantly inhibit the increased mRNA levels of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 induced by I/R. Western blot indicated that the expression of TLR4 and NF-κB were upregulated in I/R group, but OzoneOP could inhibit this increase. CONCLUSION: These findings indicated that OzoneOP had potent anti-inflammatory properties by the modulation of the TLR4-NF-κB pathway in renal ischemia/reperfusion injury. .
Asunto(s)
Animales , Masculino , Precondicionamiento Isquémico/métodos , Riñón/irrigación sanguínea , FN-kappa B/análisis , Ozono/farmacología , Daño por Reperfusión/prevención & control , /análisis , Nitrógeno de la Urea Sanguínea , Western Blotting , Creatinina/sangre , Citocinas/análisis , Inmunohistoquímica , Molécula 1 de Adhesión Intercelular/análisis , Riñón/metabolismo , FN-kappa B/metabolismo , Ratas Wistar , Reacción en Cadena en Tiempo Real de la Polimerasa , Reproducibilidad de los Resultados , Factores de Tiempo , /metabolismoRESUMEN
PURPOSE: To investigate the protective effects of ozone oxidative preconditioning (OzoneOP) were associated with the modulation of TLR4-NF-κB pathway. METHODS: Thirty six rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated and immunohistochemistry was also performed for localization of TLR4 and NF-κB. The expression of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 were studied by Real-time PCR. Western blot was performed to detect the expression of TLR4 and NF-κB. RESULTS: The results indicated that blood urea nitrogen and creatinine levels increased significantly in I/R group. Rats treated with OzoneOP showed obviously less renal damage. Immunohistochemistry showed that TLR4 were ameliorated by OzoneOP. Realtime PCR showed that OzoneOP could significantly inhibit the increased mRNA levels of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 induced by I/R. Western blot indicated that the expression of TLR4 and NF-κB were upregulated in I/R group, but OzoneOP could inhibit this increase. CONCLUSION: These findings indicated that OzoneOP had potent anti-inflammatory properties by the modulation of the TLR4-NF- κB pathway in renal ischemia/reperfusion injury.(AU)
Asunto(s)
Animales , Ratas , Ozono/análisis , Reperfusión , Isquemia , Riñón/anatomía & histología , Ratas/clasificaciónRESUMEN
Our aim was to construct a recombinant adenovirus co-expressing truncated human prostate-specific membrane antigen (tPSMA) and mouse 4-1BBL genes and to determine its effect on dendritic cells (DCs) generated from bone marrow suspensions harvested from C57BL/6 mice for which the effect of 4-1BBL on DCs is not clear, especially during DCs processing tumor-associated antigen. Replication deficient adenovirus AdMaxTM Expression System was used to construct recombinant adenovirus Ad-tPSMA-internal ribosome entry site-mouse 4-1BBL (Ad-tPSMA-IRES-m4-1BBL) and Ad-enhanced green fluorescent protein. Day 7 proliferating DC aggregates generated from C57BL/6 mice were collected as immature DCs and further mature DCs were obtained by lipopolysaccharide activated immature DCs. After DCs were exposed to the recombinant adenovirus with 250 multiplicity of infection, the expression of tPSMA and m4-1BBL proteins were detected by Western blot, and the apoptosis and phenotype of DCs were analyzed by flow cytometry. Cytokines (IL-6 and IL-12) in the supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Proliferation of T cells was detected by allogeneic mixed lymphocyte reactions. The tPSMA and m4-1BBL proteins were expressed correctly. The apoptosis rate of DCs transfected with Ad-tPSMA-IRES-m4-1BBL was 14.6 percent, lower than that of control DCs. The expression of co-stimulatory molecules [CD80 (81.6 ± 5.4 percent) and CD86 (80.13 ± 2.81 percent)] up-regulated in Ad-tPSMA-IRES-m4-1BBL-pulsed DCs, and the level of IL-6 (3960.2 ± 50.54 pg/mL) and IL-12 (249.57 ± 12.51 pg/mL) production in Ad-tPSMA-IRES-m4-1BBL-transduced DCs were significantly higher (P < 0.05) than those in control DCs. Ad-tPSMA-IRES-m4-1BBL induced higher T-cell proliferation (OD450 = 0.614 ± 0.018), indicating that this recombinant adenovirus can effectively enhance the activity of DCs.
Asunto(s)
Animales , Femenino , Humanos , Ratones , /genética , Adenoviridae/genética , Apoptosis/genética , Células Dendríticas/virología , Antígeno Prostático Específico/genética , /inmunología , Adenoviridae/inmunología , Apoptosis/inmunología , Citotoxicidad Inmunológica/inmunología , Células Dendríticas/inmunología , Células Dendríticas/patología , Ensayo de Inmunoadsorción Enzimática , Citometría de Flujo , /inmunología , /inmunología , Fenotipo , Antígeno Prostático Específico/inmunología , Proteínas Recombinantes/genética , Transducción Genética/métodosRESUMEN
Our aim was to construct a recombinant adenovirus co-expressing truncated human prostate-specific membrane antigen (tPSMA) and mouse 4-1BBL genes and to determine its effect on dendritic cells (DCs) generated from bone marrow suspensions harvested from C57BL/6 mice for which the effect of 4-1BBL on DCs is not clear, especially during DCs processing tumor-associated antigen. Replication deficient adenovirus AdMax™ Expression System was used to construct recombinant adenovirus Ad-tPSMA-internal ribosome entry site-mouse 4-1BBL (Ad-tPSMA-IRES-m4-1BBL) and Ad-enhanced green fluorescent protein. Day 7 proliferating DC aggregates generated from C57BL/6 mice were collected as immature DCs and further mature DCs were obtained by lipopolysaccharide activated immature DCs. After DCs were exposed to the recombinant adenovirus with 250 multiplicity of infection, the expression of tPSMA and m4-1BBL proteins were detected by Western blot, and the apoptosis and phenotype of DCs were analyzed by flow cytometry. Cytokines (IL-6 and IL-12) in the supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Proliferation of T cells was detected by allogeneic mixed lymphocyte reactions. The tPSMA and m4-1BBL proteins were expressed correctly. The apoptosis rate of DCs transfected with Ad-tPSMA-IRES-m4-1BBL was 14.6%, lower than that of control DCs. The expression of co-stimulatory molecules [CD80 (81.6 ± 5.4%) and CD86 (80.13 ± 2.81%)] up-regulated in Ad-tPSMA-IRES-m4-1BBL-pulsed DCs, and the level of IL-6 (3960.2 ± 50.54 pg/mL) and IL-12 (249.57 ± 12.51 pg/mL) production in Ad-tPSMA-IRES-m4-1BBL-transduced DCs were significantly higher (P < 0.05) than those in control DCs. Ad-tPSMA-IRES-m4-1BBL induced higher T-cell proliferation (OD(450) = 0.614 ± 0.018), indicating that this recombinant adenovirus can effectively enhance the activity of DCs.