Limb ischemic preconditioning via activation of mitogen-activated protein kinase p38 reduce cerebral ischemia induced hippocampal CA1 neuronal apoptosis and cerebral edema
Purpose was to investigate limb ischemic preconditioning (LIP) process can reduce cerebral ischemic hippocampal CA1 neuronal apoptosis and cerebral edema. Methods 72 permanently occluded vertebral artery Wistar rats were randomly divided into six groups: sham, LIP (bilateral femoral artery occlusion 10min, intermittent 10min, 3 cycles), cerebral ischemia, LIP + cerebral ischemia, DMSO and SB 203580 + LIP + cerebral ischemia group. 6 rats in each group after cerebral ischemia 3d death, TUNEL staining of apoptotic cells counted; 6 sacrificed 24h after cerebral ischemia, brain water content was measured. TUNEL staining results showed that sham and LIP group hippocampal CA1 occasional TUNEL-positive cells; cerebral ischemic hippocampal CA1 region shows a large brown colored TUNEL-positive cells, with the sham group and LIP group compared to the number of cells increased significantly ; LIP + cerebral ischemia group, TUNEL-positive neurons compared with cerebral ischemia group was significantly reduced, suggesting that LIP significantly inhibited ischemia-induced hippocampal CA1 pyramidal cells; mitogen-activated protein kinase p38 antagonist SB 203580 + LIP + cerebral ischemia group, positive staining of hippocampal CA1 pyramidal cells increased significantly, with DMSO + LIP + cerebral ischemia group had significant difference compared with that SB 203580 could antagonize LIP inhibition of apoptosis. With the sham and LIP group, ischemic brain tissue water content was significantly increased, indicating that LIP reduces ischemic brain tissue caused by increased water content; LIP LIP before the application of SB 203580 inhibit cerebral protection, the brain tissue water content than the LIP + cerebral ischemia group increased significantly. Conclusion LIP process can reduce ischemic hippocampal CA1 neuronal apoptosis and cerebral edema, may be associated with activation of mitogen-activated protein kinase p38 related.
Limb ischemic preconditioning via activation of mitogen-activated protein kinase p38 reduce cerebral ischemia induced hippocampal CA1 neuronal apoptosis and cerebral edema
ReplyDeletePurpose was to investigate limb ischemic preconditioning (LIP) process can reduce cerebral ischemic hippocampal CA1 neuronal apoptosis and cerebral edema. Methods 72 permanently occluded vertebral artery Wistar rats were randomly divided into six groups: sham, LIP (bilateral femoral artery occlusion 10min, intermittent 10min, 3 cycles), cerebral ischemia, LIP + cerebral ischemia, DMSO and SB 203580 + LIP + cerebral ischemia group. 6 rats in each group after cerebral ischemia 3d death, TUNEL staining of apoptotic cells counted; 6 sacrificed 24h after cerebral ischemia, brain water content was measured. TUNEL staining results showed that sham and LIP group hippocampal CA1 occasional TUNEL-positive cells; cerebral ischemic hippocampal CA1 region shows a large brown colored TUNEL-positive cells, with the sham group and LIP group compared to the number of cells increased significantly ; LIP + cerebral ischemia group, TUNEL-positive neurons compared with cerebral ischemia group was significantly reduced, suggesting that LIP significantly inhibited ischemia-induced hippocampal CA1 pyramidal cells; mitogen-activated protein kinase p38 antagonist SB 203580 + LIP + cerebral ischemia group, positive staining of hippocampal CA1 pyramidal cells increased significantly, with DMSO + LIP + cerebral ischemia group had significant difference compared with that SB 203580 could antagonize LIP inhibition of apoptosis. With the sham and LIP group, ischemic brain tissue water content was significantly increased, indicating that LIP reduces ischemic brain tissue caused by increased water content; LIP LIP before the application of SB 203580 inhibit cerebral protection, the brain tissue water content than the LIP + cerebral ischemia group increased significantly. Conclusion LIP process can reduce ischemic hippocampal CA1 neuronal apoptosis and cerebral edema, may be associated with activation of mitogen-activated protein kinase p38 related.
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