Effect of ischemic preconditioning on apoptosis proliferation and Bcl-2 expression in acute renal ischemia/ reperfusion rats
Yang Xu
Abstract
Yang Xu
Abstract
AIM: To investigate the effects of ischemic preconditioning (IPC) on apoptosis, proliferation and Bcl 2 expression known to modulate apoptosis induced by acute renal ischemia/reperfusion. METHODS: Fifty healthy Wistar male rats weighing (250±30) g were anesthetized with 100 mL·L -1 hydratrion chorincalaehyde 0.3 mL and randomly divided into five equal groups with ten animals each. The kidney ischemic preconditioning was induced by circles of left renal ischemia (8 min) separated by reperfusion (5 min) before ischemia reperfusion injury. Right kidneys were removed except group A and ischemia was induced by clamping the left renal pendicle for 45 min by using a nontraumtic vas through a tranverse abdominal incision. The expression of Bcl 2 was observed by immunohistochemistry (SABC) and cell apoptosis and proliferation in the rats were assayed by flow cytometry. RESULTS: The percentage of apoptosis in the I/R group was significantly higher than that in the normal and shame groups ( P 0.01). IPC decreased the percentage of apoptosis and increased A (absorbance) value of bcl 2 protein and the cells of G 0/G 1 phase in the cell cycle as compared with the I/R group. I/R increased the percentage of apoptosis as compared with the ischemia group. CONCLUSION: Apoptosis obviously increases in I/R group and IPC can inhibit the apoptosis induced by renal I/R through upregulating the expression of bcl 2 or modulating the proliferation.
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AIM: To investigate the effects of ischemic preconditioning (IPC) on apoptosis, proliferation and Bcl 2 expression known to modulate apoptosis induced by acute renal ischemia/reperfusion. METHODS: Fifty healthy Wistar male rats weighing (250±30) g were anesthetized with 100 mL·L -1 hydratrion chorincalaehyde 0.3 mL and randomly divided into five equal groups with ten animals each. The kidney ischemic preconditioning was induced by circles of left renal ischemia (8 min) separated by reperfusion (5 min) before ischemia reperfusion injury. Right kidneys were removed except group A and ischemia was induced by clamping the left renal pendicle for 45 min by using a nontraumtic vas through a tranverse abdominal incision. The expression of Bcl 2 was observed by immunohistochemistry (SABC) and cell apoptosis and proliferation in the rats were assayed by flow cytometry. RESULTS: The percentage of apoptosis in the I/R group was significantly higher than that in the normal and shame groups ( P 0.01). IPC decreased the percentage of apoptosis and increased A (absorbance) value of bcl 2 protein and the cells of G 0/G 1 phase in the cell cycle as compared with the I/R group. I/R increased the percentage of apoptosis as compared with the ischemia group. CONCLUSION: Apoptosis obviously increases in I/R group and IPC can inhibit the apoptosis induced by renal I/R through upregulating the expression of bcl 2 or modulating the proliferation.
Key concepts: Apoptosis, Ischemic preconditioning, Ischemia, Renal ischemia, Medicine, Kidney, Flow cytometry, Endocrinology