Objective ：To study the differences in expression of nuclear factor-κB （NF-κB） between human traumatic cataract and normal lenticular epithelial cells. Methods： Total RNA of anterior capsule specimens was taken...Objective ：To study the differences in expression of nuclear factor-κB （NF-κB） between human traumatic cataract and normal lenticular epithelial cells. Methods： Total RNA of anterior capsule specimens was taken under the microscope from normal cadaveric eyes donors and those suffering from traumatic cataract to make semi-quantitative RT-PCR and conduct analysis of differences in expression of NF-κB between them. Results： As compared with the mean of 0.8337 in normal control group, the expression equivalent of NF-κB was 0. 9074 for the lenticular epithelial cells in traumatic cataract sufferers, and the differences are of noticeable significance （ t = 2.447, P 〈 0.05） accordingly. Conclusions： NF-κB is likely a kind of transcription factor necessary to maintain metabolism of normal lenticular epithelial cells. Higher NF-κB available in the traumatic cataract sufferer＇s lenticular epithelial cells means NF-κB is of possible relevance to occurrence and development of traumatic cataract.展开更多
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 (th...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.展开更多
文摘Objective ：To study the differences in expression of nuclear factor-κB （NF-κB） between human traumatic cataract and normal lenticular epithelial cells. Methods： Total RNA of anterior capsule specimens was taken under the microscope from normal cadaveric eyes donors and those suffering from traumatic cataract to make semi-quantitative RT-PCR and conduct analysis of differences in expression of NF-κB between them. Results： As compared with the mean of 0.8337 in normal control group, the expression equivalent of NF-κB was 0. 9074 for the lenticular epithelial cells in traumatic cataract sufferers, and the differences are of noticeable significance （ t = 2.447, P 〈 0.05） accordingly. Conclusions： NF-κB is likely a kind of transcription factor necessary to maintain metabolism of normal lenticular epithelial cells. Higher NF-κB available in the traumatic cataract sufferer＇s lenticular epithelial cells means NF-κB is of possible relevance to occurrence and development of traumatic cataract.
文摘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.
