Expression of P-erk and neuron apoptosis in model of focal cerebral ischemia-reperfusion rats
Baoming Xie
Abstract
Baoming Xie
Abstract
Objective To explore the expression of P-erk(phospho-excelluar signal-regulated kinase)in the model rats of focal cerebral ischemia-reperfusion. Methods The model of focal cerebral ischemia-reperfusion injury was made.The histopathological changes of brain tissue were observed by HE staining.The P-erk protein expression was detected by immunohistochemistry.The neuronal apoptosis was detected by TUNEL Apoptosis Detection Kit. Results ①Expression of P-erk positive cells was found in the central core of the infarction and the penumbra zone after cerebral ischemia followed by reperfusion,peaked at 6 h after reperfusion,and then declined at 12 h after reperfusion.②Expression of TUNEL positive cells was found in the central core of infarction penumbra zone after cerebral ischemia followed by reperfusion, and the expression increased significantly at 24 h after reperfusion,and peaked at 48 h. Conclusion The expression of P-erk protein may participate in the occurrence of ischemic cellular injury by inducing apoptosis and non-apoptotic programmed neuronal death.
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Objective To explore the expression of P-erk(phospho-excelluar signal-regulated kinase)in the model rats of focal cerebral ischemia-reperfusion. Methods The model of focal cerebral ischemia-reperfusion injury was made.The histopathological changes of brain tissue were observed by HE staining.The P-erk protein expression was detected by immunohistochemistry.The neuronal apoptosis was detected by TUNEL Apoptosis Detection Kit. Results ①Expression of P-erk positive cells was found in the central core of the infarction and the penumbra zone after cerebral ischemia followed by reperfusion,peaked at 6 h after reperfusion,and then declined at 12 h after reperfusion.②Expression of TUNEL positive cells was found in the central core of infarction penumbra zone after cerebral ischemia followed by reperfusion, and the expression increased significantly at 24 h after reperfusion,and peaked at 48 h. Conclusion The expression of P-erk protein may participate in the occurrence of ischemic cellular injury by inducing apoptosis and non-apoptotic programmed neuronal death.
Key concepts: Penumbra, TUNEL assay, Ischemia, Apoptosis, MAPK/ERK pathway, Medicine, Immunohistochemistry, Reperfusion injury