PDF(Pubmed)
Abstract：
UNASSIGNED: Insulin attaches insulin receptor to activate the PI3-kinase/Akt signaling to maintain glucose homeostasis and inhibit apoptosis. This study determined whether preconditioning with insulin and glucose protects the kidney against ischemia-reperfusion injury (IRI).
UNASSIGNED: Kidney IRI was performed in C57BL/6 mice by clamping the renal vessels for 30 min, followed by reperfusion for 24 h. A total subcutaneous 0.1 unit of insulin along with 10% glucose in drinking water was treated on the mice for 24 h before kidney IRI. The kidney function and injuries were investigated through the determination of BUN and Cr in blood plasma, as well as the apoptosis and the expression of P-AKT, BAX, and caspase-3 in the kidneys. The role of P-AKT in insulin-treated IRI kidneys was tested using an AKT inhibitor. The effects of the preconditional duration of insulin and glucose on IRI kidneys were investigated by expanding the treatment duration to 1, 3, and 6 days.
UNASSIGNED: Preconditioning with insulin and glucose protected the kidney against IRI as manifested by a decrease in creatinine and BUN and a reduction of kidney tubular injury. The protection effect was mediated by P-AKT-BAX-caspase-3 signaling pathway resulting in suppression of apoptotic cell death. An AKT inhibitor partially reversed the protective effects of preconditional insulin. The preconditional duration for 1, 3, and 6 days had no differences in improving kidney functions and pathology.
UNASSIGNED: A short-term preconditioning with insulin and glucose protected the kidney from IRI through the activation of p-AKT and subsequent reduction of BAX-caspase-3-induced apoptosis. The short-term precondition provides a practicable strategy for protecting the kidney against predictable IRI, such as kidney transplant and major surgical operations with high risk of hypotension.
UNASSIGNED: Kidney IRI was performed in C57BL/6 mice by clamping the renal vessels for 30 min, followed by reperfusion for 24 h. A total subcutaneous 0.1 unit of insulin along with 10% glucose in drinking water was treated on the mice for 24 h before kidney IRI. The kidney function and injuries were investigated through the determination of BUN and Cr in blood plasma, as well as the apoptosis and the expression of P-AKT, BAX, and caspase-3 in the kidneys. The role of P-AKT in insulin-treated IRI kidneys was tested using an AKT inhibitor. The effects of the preconditional duration of insulin and glucose on IRI kidneys were investigated by expanding the treatment duration to 1, 3, and 6 days.
UNASSIGNED: Preconditioning with insulin and glucose protected the kidney against IRI as manifested by a decrease in creatinine and BUN and a reduction of kidney tubular injury. The protection effect was mediated by P-AKT-BAX-caspase-3 signaling pathway resulting in suppression of apoptotic cell death. An AKT inhibitor partially reversed the protective effects of preconditional insulin. The preconditional duration for 1, 3, and 6 days had no differences in improving kidney functions and pathology.
UNASSIGNED: A short-term preconditioning with insulin and glucose protected the kidney from IRI through the activation of p-AKT and subsequent reduction of BAX-caspase-3-induced apoptosis. The short-term precondition provides a practicable strategy for protecting the kidney against predictable IRI, such as kidney transplant and major surgical operations with high risk of hypotension.
摘要：
■胰岛素附着胰岛素受体以激活PI3-激酶/Akt信号传导以维持葡萄糖稳态并抑制细胞凋亡。这项研究确定了胰岛素和葡萄糖预处理是否可以保护肾脏免受缺血再灌注损伤（IRI）。
■在C57BL/6小鼠中通过夹住肾血管30分钟进行肾IRI，然后再灌注24小时。在肾脏IRI之前，对小鼠进行皮下总0.1单位的胰岛素以及饮用水中的10％葡萄糖处理24小时。通过测定血浆中的BUN和Cr，研究肾功能和损伤。以及细胞凋亡和P-AKT的表达，巴克斯，和caspase-3在肾脏。使用AKT抑制剂测试了P-AKT在胰岛素治疗的IRI肾脏中的作用。通过将治疗持续时间扩展至1、3和6天来研究胰岛素和葡萄糖的先决条件持续时间对IRI肾脏的影响。
■用胰岛素和葡萄糖预处理可保护肾脏免受IRI，表现为肌酐和BUN减少以及肾小管损伤减少。保护作用由P-AKT-BAX-caspase-3信号通路介导,导致凋亡细胞死亡的抑制。AKT抑制剂部分逆转了先决条件胰岛素的保护作用。1、3和6天的先决条件持续时间在改善肾功能和病理方面没有差异。
■胰岛素和葡萄糖的短期预处理通过激活p-AKT和随后减少BAX-caspase-3诱导的细胞凋亡来保护肾脏免受IRI。短期先决条件为保护肾脏免受可预测的IRI提供了可行的策略，如肾移植和低血压高风险的大型外科手术。
■在C57BL/6小鼠中通过夹住肾血管30分钟进行肾IRI，然后再灌注24小时。在肾脏IRI之前，对小鼠进行皮下总0.1单位的胰岛素以及饮用水中的10％葡萄糖处理24小时。通过测定血浆中的BUN和Cr，研究肾功能和损伤。以及细胞凋亡和P-AKT的表达，巴克斯，和caspase-3在肾脏。使用AKT抑制剂测试了P-AKT在胰岛素治疗的IRI肾脏中的作用。通过将治疗持续时间扩展至1、3和6天来研究胰岛素和葡萄糖的先决条件持续时间对IRI肾脏的影响。
■用胰岛素和葡萄糖预处理可保护肾脏免受IRI，表现为肌酐和BUN减少以及肾小管损伤减少。保护作用由P-AKT-BAX-caspase-3信号通路介导,导致凋亡细胞死亡的抑制。AKT抑制剂部分逆转了先决条件胰岛素的保护作用。1、3和6天的先决条件持续时间在改善肾功能和病理方面没有差异。
■胰岛素和葡萄糖的短期预处理通过激活p-AKT和随后减少BAX-caspase-3诱导的细胞凋亡来保护肾脏免受IRI。短期先决条件为保护肾脏免受可预测的IRI提供了可行的策略，如肾移植和低血压高风险的大型外科手术。
