Effect of acute high glucose condition on renal ischemia reperfusion injury in rats and the preconditioning effect of dexmedetomidine
Min Liu, Huaxin Wang, Bo Zhao, Yeda Xiao, Kang Liu
Abstract
Min Liu, Huaxin Wang, Bo Zhao, Yeda Xiao, Kang Liu
Abstract
Objective To investigate the effect of acute high glucose on renal ischemia reperfusion injury in rats and the preconditioning effect of dexmedetomidine (Dex). Methods Sixty SD rats were divided into 6 groups: NG-Sham group, NG-I/R group, NG-Dex group, HG-Sham group, HG-I/R group, HG-Dex group. Renal ischemia reperfusion model was made, and the Dex preconditioning groups were given Dex 50 μg/kg intraperitoneally 30 min before ischemia. The kidney was removed for histopathologic examination. Blood urea nitrogen (BUN) and creatinine (Cr) were determined. The apoptosis was tested by TdT-mediated dUTP nick end labeling (TUNEL). B cell lymphoma/leukemia-2 associated X protein (bax), B cell lymphoma/leukemia-2 (bcl-2), protein kinase B (Akt) , and phosphorylated protein kinase B (p-Akt) were detected by Western blotting. Results Compared with NG-Sham group, BUN [(7.41±0.16) mmol/L vs. (20.24±2.94) mmol/L], Cr [(31.25±2.44) μmol/L vs. (76.50±3.59) μmol/L], TUNEL (1.88±0.64 vs. 35.88±2.70), bax (0.21±0.03 vs. 0.62±0.01) and p-Akt (0.11±0.01 vs. 0.31±0.03) in NG-I/R group were higher, bcl-2 (0.52±0.03 vs. 0.20±0.01) was decreased (P 0.05). Conclusion Dex has a protective effect on renal ischemia reperfusion injury, but this effect is inhibited in high glucose condition, which may be related to the expression of p-Akt, bax and bcl-2. Key words: High glucose; Renal ischemia reperfusion injury; Dexmedetomidine; Preconditioning
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Objective To investigate the effect of acute high glucose on renal ischemia reperfusion injury in rats and the preconditioning effect of dexmedetomidine (Dex). Methods Sixty SD rats were divided into 6 groups: NG-Sham group, NG-I/R group, NG-Dex group, HG-Sham group, HG-I/R group, HG-Dex group. Renal ischemia reperfusion model was made, and the Dex preconditioning groups were given Dex 50 μg/kg intraperitoneally 30 min before ischemia. The kidney was removed for histopathologic examination. Blood urea nitrogen (BUN) and creatinine (Cr) were determined. The apoptosis was tested by TdT-mediated dUTP nick end labeling (TUNEL). B cell lymphoma/leukemia-2 associated X protein (bax), B cell lymphoma/leukemia-2 (bcl-2), protein kinase B (Akt) , and phosphorylated protein kinase B (p-Akt) were detected by Western blotting. Results Compared with NG-Sham group, BUN [(7.41±0.16) mmol/L vs. (20.24±2.94) mmol/L], Cr [(31.25±2.44) μmol/L vs. (76.50±3.59) μmol/L], TUNEL (1.88±0.64 vs. 35.88±2.70), bax (0.21±0.03 vs. 0.62±0.01) and p-Akt (0.11±0.01 vs. 0.31±0.03) in NG-I/R group were higher, bcl-2 (0.52±0.03 vs. 0.20±0.01) was decreased (P 0.05). Conclusion Dex has a protective effect on renal ischemia reperfusion injury, but this effect is inhibited in high glucose condition, which may be related to the expression of p-Akt, bax and bcl-2. Key words: High glucose; Renal ischemia reperfusion injury; Dexmedetomidine; Preconditioning
Key concepts: TUNEL assay, Creatinine, Blood urea nitrogen, Protein kinase B, Endocrinology, Reperfusion injury, Internal medicine, Apoptosis