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Objective: To explore the relationship between neuronal apoptosis and hypoxia or traumatic injury. Methods: Rat neurons primarily cultured in vitro were treated with hypoxia (the hypoxia group) or traumatic injury (the trauma group). The neuronal apoptosis was evaluated with microscope, TUNEL (terminal deoxynucleotidyl transferase mediated X dUTPnick end labeling) staining, flow cytometry, agarose gel electrophoresis and immunohistochemistry. Results: Morphological changes of apoptosis appeared in the treated neurons,and the DNA fragmentation showed “ladder” break. The apoptotic index was 10.8% in the hypoxia group and 4.8% in the trauma group, while it was only 1.6% in the control group. The expression of apoptosis associated genes (c myc, fas and fasL) increased.Conclusions: Hypoxia or traumatic injury can induce neuronal apoptosis, and its molecular mechanism is probably related to the expressions of apoptosis associated genes.
Methods: Rat neurons in cultured in vitro were treated with hypoxia (the hypoxia group) or traumatic injury (the trauma group). The neuronal apoptosis was evaluated with microscope, TUNEL Results: Morphological changes of apoptosis were in the treated neurons, and the DNA fragmentation showed “ladder” break. The apoptotic index was 10.8% in the hypoxia group and 4.8% in the trauma group, while it was only 1.6% in the control group. The expression of apoptosis associated genes (c myc, fas and fasL) increased. Conclusions: Hypoxia or traumatic injury can induce neuronal apoptosis, and its molecular mechanism is probably related to the expressions of apoptosis associated genes.