ABSTRACT
PURPOSE: To investigate the effect of ozone oxidative preconditioning (OzoneOP) on inflammation and oxidative stress injury in rat model of renal transplantation. METHODS: Thirty six male Sprague Dawley (SD) rats were randomly divided into three groups. Sham group: rats were treated with opening and closing abdomen. Kidney transplantation group (KT group): SD rat received the donor's left kidney derived from another SD rat. Ozone oxidative preconditioning and kidney transplantation (OOP+KT group): donor SD rats received OzoneOP treatments by transrectal insufflations before kidney transplantation. After transplantation, parameters of renal function of recipients were determined. Morphology and pathological changes of renal allograft were examined. Expression of NF-κBp65, HMGB-1 were also determined by Western-blot. RESULTS: Compared to KT group, the morphology and pathological damages of renal allograft were less serious in OOP+KT group. Meanwhile, levels of SOD and GSH-Px of renal allograft in OOP+KT group were higher than those in KT group respectively. Western-blot showed that the expressions of NF-κBp65 and HMGB-1 in OOP+KT group were obviously less than those in KT group. CONCLUSION: Ozone oxidative preconditioning could attenuate the inflammatory reaction and oxidative stress injury in renal allograft, which might be related with the enhancement of anti-oxidative system and suppression of inflammatory reaction.
Subject(s)
Inflammation/prevention & control , Ischemic Preconditioning/methods , Kidney Transplantation/methods , Ozone/administration & dosage , Animals , Blotting, Western , Inflammation/etiology , Kidney Transplantation/adverse effects , Male , Models, Animal , Oxidation-Reduction/drug effects , Oxidative Stress/drug effects , Rats , Rats, Sprague-Dawley , Reperfusion Injury/prevention & control , Superoxide Dismutase/metabolismABSTRACT
Abstract Purpose: To investigate the effect of ozone oxidative preconditioning (OzoneOP) on inflammation and oxidative stress injury in rat model of renal transplantation. Methods: Thirty six male Sprague Dawley (SD) rats were randomly divided into three groups. Sham group: rats were treated with opening and closing abdomen. Kidney transplantation group (KT group): SD rat received the donor's left kidney derived from another SD rat. Ozone oxidative preconditioning and kidney transplantation (OOP+KT group): donor SD rats received OzoneOP treatments by transrectal insufflations before kidney transplantation. After transplantation, parameters of renal function of recipients were determined. Morphology and pathological changes of renal allograft were examined. Expression of NF-κBp65, HMGB-1 were also determined by Western-blot. Results: Compared to KT group, the morphology and pathological damages of renal allograft were less serious in OOP+KT group. Meanwhile, levels of SOD and GSH-Px of renal allograft in OOP+KT group were higher than those in KT group respectively. Western-blot showed that the expressions of NF-κBp65 and HMGB-1 in OOP+KT group were obviously less than those in KT group. Conclusion: Ozone oxidative preconditioning could attenuate the inflammatory reaction and oxidative stress injury in renal allograft, which might be related with the enhancement of anti-oxidative system and suppression of inflammatory reaction.
Subject(s)
Animals , Male , Rats , Ozone/administration & dosage , Kidney Transplantation/methods , Ischemic Preconditioning/methods , Inflammation/prevention & control , Oxidation-Reduction/drug effects , Superoxide Dismutase/metabolism , Reperfusion Injury/prevention & control , Blotting, Western , Kidney Transplantation/adverse effects , Rats, Sprague-Dawley , Oxidative Stress/drug effects , Models, Animal , Inflammation/etiologyABSTRACT
Purpose: To investigate the effect of ozone oxidative preconditioning (OzoneOP) on inflammation and oxidative stress injury in rat model of renal transplantation. Methods: Thirty six male Sprague Dawley (SD) rats were randomly divided into three groups. Sham group: rats were treated with opening and closing abdomen. Kidney transplantation group (KT group): SD rat received the donors left kidney derived from another SD rat. Ozone oxidative preconditioning and kidney transplantation (OOP+KT group): donor SD rats received OzoneOP treatments by transrectal insufflations before kidney transplantation. After transplantation, parameters of renal function of recipients were determined. Morphology and pathological changes of renal allograft were examined. Expression of NF-kBp65, HMGB-1 were also determined by Western-blot. Results: Compared to KT group, the morphology and pathological damages of renal allograft were less serious in OOP+KT group. Meanwhile, levels of SOD and GSH-Px of renal allograft in OOP+KT group were higher than those in KT group respectively. Western-blot showed that the expressions of NF-kBp65 and HMGB-1 in OOP+KT group were obviously less than those in KT group. Conclusion: Ozone oxidative preconditioning could attenuate the inflammatory reaction and oxidative stress injury in renal allograft, which might be related with the enhancement of anti-oxidative system and suppression of inflammatory reaction.(AU)
Subject(s)
Animals , Rats , Ozone , Kidney Transplantation , Oxidative Stress , ResearchABSTRACT
PURPOSE: To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS: Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS: Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION: Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.
Subject(s)
Allopurinol/pharmacology , HMGB1 Protein/drug effects , Ischemic Preconditioning/methods , Kidney/blood supply , Protective Agents/pharmacology , Reperfusion Injury/prevention & control , Animals , Apoptosis/drug effects , Blood Urea Nitrogen , Disease Models, Animal , HMGB1 Protein/metabolism , Inflammation/metabolism , Kidney/pathology , Male , Peroxidase/metabolism , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Superoxide Dismutase/drug effectsABSTRACT
ABSTRACT PURPOSE: To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS: Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS: Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION: Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.
Subject(s)
Animals , Male , Reperfusion Injury/prevention & control , Allopurinol/pharmacology , Ischemic Preconditioning/methods , Protective Agents/pharmacology , HMGB1 Protein/drug effects , Kidney/blood supply , Superoxide Dismutase/drug effects , Blood Urea Nitrogen , Reperfusion Injury/metabolism , Random Allocation , Rats, Sprague-Dawley , Apoptosis/drug effects , Peroxidase/metabolism , HMGB1 Protein/metabolism , Disease Models, Animal , Inflammation/metabolism , Kidney/pathologyABSTRACT
PURPOSE:To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model.METHODS:Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis.RESULTS:Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05).CONCLUSION:Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.(AU)
Subject(s)
Animals , Rats , Allopurinol/therapeutic use , Reperfusion Injury/therapy , Reperfusion Injury/veterinary , HMGB1 Protein , Kidney/injuries , ApoptosisABSTRACT
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.
Subject(s)
Apoptosis/drug effects , Epithelial Cells/drug effects , Ischemic Preconditioning/methods , Kidney/blood supply , Kidney/drug effects , Metformin/pharmacology , Reperfusion Injury/prevention & control , AMP-Activated Protein Kinases/analysis , Animals , Blood Urea Nitrogen , Blotting, Western , Caspase 3/analysis , Creatinine/blood , Cyclooxygenase 2/analysis , Immunohistochemistry , Kidney/pathology , Male , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Time FactorsABSTRACT
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)
Subject(s)
Animals , Male , Apoptosis , Epithelial Cells , Ischemic Preconditioning/methods , Kidney/blood supply , Kidney , Metformin/pharmacology , Reperfusion Injury/prevention & control , AMP-Activated Protein Kinases/analysis , Blood Urea Nitrogen , Blotting, Western , Caspase 3/analysis , Creatinine/blood , Cyclooxygenase 2/analysis , Immunohistochemistry , Kidney/pathology , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Time FactorsABSTRACT
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.
Subject(s)
Animals , Male , Apoptosis/drug effects , Epithelial Cells/drug effects , Ischemic Preconditioning/methods , Kidney/blood supply , Kidney/drug effects , Metformin/pharmacology , Reperfusion Injury/prevention & control , AMP-Activated Protein Kinases/analysis , Blood Urea Nitrogen , Blotting, Western , /analysis , Creatinine/blood , /analysis , Immunohistochemistry , Kidney/pathology , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Time FactorsABSTRACT
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.
Subject(s)
Alkaloids/pharmacology , Antioxidants/pharmacology , Heme Oxygenase-1/metabolism , Kidney/blood supply , NF-E2-Related Factor 2/metabolism , Oxidative Stress/drug effects , Quinolizines/pharmacology , Reperfusion Injury/prevention & control , Alkaloids/therapeutic use , Animals , Antioxidants/therapeutic use , Apoptosis/drug effects , Blotting, Western , Disease Models, Animal , Heme Oxygenase-1/analysis , Immunohistochemistry , In Situ Nick-End Labeling , Kidney/pathology , Male , NF-E2-Related Factor 2/analysis , Quinolizines/therapeutic use , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Reperfusion Injury/pathology , Reproducibility of Results , Time Factors , Treatment OutcomeABSTRACT
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. .
Subject(s)
Animals , Male , Alkaloids/pharmacology , Antioxidants/pharmacology , Heme Oxygenase-1/metabolism , Kidney/blood supply , /metabolism , Oxidative Stress/drug effects , Quinolizines/pharmacology , Reperfusion Injury/prevention & control , Alkaloids/therapeutic use , Antioxidants/therapeutic use , Apoptosis/drug effects , Blotting, Western , Disease Models, Animal , Heme Oxygenase-1/analysis , Immunohistochemistry , In Situ Nick-End Labeling , Kidney/pathology , /analysis , Quinolizines/therapeutic use , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Reperfusion Injury/metabolism , Reperfusion Injury/pathology , Time Factors , Treatment OutcomeABSTRACT
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)