Hippocampal expression of apoptotic protease activating factor-1 following diffuse axonal injury under mild hypothermia

The influence of mild hypothermia on neural cell apoptosis remains poorly understood. Therefore, the present study established rat models of diffuse axonal injury （DAI） at 33℃. Morris water maze results demonstrated significantly better learning and memory functions in DAI rats with hypothermia compared with DAI rats with normothermia. Expression of apoptotic protease activating factor-1 in the hippocampal CA1 region was significantly lower in the DAI hypothermia group compared with the DAI normothermia group. Expression of apoptotic protease activating factor-1 positively correlated with latency, but negatively correlated with platform location times and time of swimming in the quadrant area. Results suggested that post-traumatic mild hypothermia in a rat model of DAI could provide cerebral protection by attenuating expression of apoptotic protease activating factor-1.

Procaine Inhibiting Human Bladder Cancer Cell Proliferation by Inducing Apoptosis and Demethylating APAF1 CpG Island Hypermethylated

Studies have shown that aberrant DNA methylation of apoptotic protease activating factor-1（APAF1） is an important epigenetic mechanism of gene regulation in the progression of bladder cancer.In this article,we have proved that procaine,an inhibitor of DNA methyltransferases,could inhibit the proliferation of T24 and 5637 human bladder cancer cells by inducing their apoptosis.The mechanism studies reveal that procaine could induce demethylation of APAF1 gene in T24 or 5637 cells,subsequently activating caspase-3/9.It was also shown that the serum soluble fas ligand（sFasL） was activated,and the expression of matrix metallopeptidase 9（MMP-9） was down-regulated.Procaine seems to induce cell death by different pathways,and it might be used as a potential agent for bladder cancer treatment.

头孢曲松对大鼠弥漫性轴索损伤后细胞凋亡的影响

目的探讨头孢曲松对大鼠弥漫性轴索损伤后海马CA1区神经元凋亡的影响。方法选择雄性Wistar大鼠120只,随机分为药物干预组(n=36):制作弥漫性轴索损伤模型,于制作模型后即刻给予头孢曲松200 mg·kg-1。假手术组(n=36):仅行头皮切开缝合处理,给予等量生理盐水腹腔注射。脑损伤组(n=36):制作弥漫性轴索损伤模型,给予等量生理盐水腹腔注射。正常对照组(n=12):不给予任何干预措施。采用免疫组化技术检测干预后12、24和36h时相海马CA1区凋亡蛋白酶激活因子-1(Apaf-1)蛋白的表达水平。结果脑损伤组和药物干预组大鼠海马CA1区Apaf-1蛋白表达水平均于12 h开始增加,24 h达高峰,此后逐渐下降。药物干预组大鼠海马CA1区Apaf-1蛋白表达水平在各个时相点均低于脑损伤组,均差异有统计学意义。结论弥漫性轴索损伤可引起大鼠海马CA1区神经元凋亡,头孢曲松可改善凋亡的发生、发展。