Objective To establish an artificial somatic-autonomic reflex arc in rats and observe the following distributive changes of neural fibers in the bladder. Methods Adult Sprague-Dawley rats were randomly divided into th...
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Objective To establish an artificial somatic-autonomic reflex arc in rats and observe the following distributive changes of neural fibers in the bladder. Methods Adult Sprague-Dawley rats were randomly divided into three groups： control group, spinal cord injury （SCI） group, and reinnervation group. DiI retrograde tracing was used to verify establishment of the model and to investigate the transport function of the regenerated efferent axons in the new reflex arc. Choline acetyltransferase （CHAT） in the DiI-labeled neurons was detected by immunohistochemistry. Distribution of neural fibers in the bladder was observed by acetylcholine esterase staining. Results DR-labeled neurons distributed mainly in the left ventral horn from L3 to L5, and some of them were also CHAT-positive. The neural fibers in the bladder detrusor reduced remarkably in the SCI group compared with the control （P 〈 0.05）. After establishment of the somatic-autonomic reflex arc in the reinnervation group, the number of ipsilateral fibers in the bladder increased markedly compared with the SCI group （P 〈 0.05）, though still much less than that in the control （P 〈 0.05）. Conclusion The efferent branches of the somatic nerves may grow and replace the parasympathetic preganglionic axons through axonal regeneration. Acetylcholine is still the major neurotransmitter of the new reflex arc. The controllability of detrusor may be promoted when it is reinnervated by the pelvic ganglia efferent somatic motor fibers from the postganglionic axons.
目的：研究多种细胞因子诱导的杀伤细胞（cytokine-induced killing cells,CIK）对乳腺癌细胞株ZK-75-1的杀伤作用,并探讨其作用机制.方法：通过HE染色观察凋亡细胞ZK-75-1的形态学改变.应用TUNEL（TdT-mediated dUTPnick end labeling...
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目的：研究多种细胞因子诱导的杀伤细胞（cytokine-induced killing cells,CIK）对乳腺癌细胞株ZK-75-1的杀伤作用,并探讨其作用机制.方法：通过HE染色观察凋亡细胞ZK-75-1的形态学改变.应用TUNEL（TdT-mediated dUTPnick end labeling）法检测CIK细胞的凋亡.通过免疫细胞化学染色法检测ZK-75-1细胞中p53、p16、C-myc、Bcl-2及Bax的表达率.结果：HE染色显示,CIK细胞向ZK-75-1细胞靠近,形成典型的玫瑰花环状;肿瘤细胞的胞浆中出现颗粒状物,有的肿瘤细胞只见颗粒状碎片;而作为对照的乳腺癌细胞生长良好.TUNEL法检测显示,对照组细胞未染色或染呈均匀的淡蓝色;实验组凋亡的细胞缩小,核或核周染呈深蓝色.CIK细胞作用4～12 h ZK-75-1细胞的凋亡率上升,作用12～24h细胞的凋亡率下降,与对照组相比较有统计学意义（P＜0.01）.免疫细胞化学染色的结果表明,CIK细胞实验组p53、pi6、C-myc及Bcl-2蛋白随作用时间的延长均下降,Bax蛋白的表达上调,与对照组相比较均有统计学意义（P＜0.01）.结论：CIK细胞对乳腺癌细胞ZK-75-1杀伤作用的机制之一,可能与p53、p16、C-myc、Bcl-2蛋白表达的下调及Bax蛋白表达的上调有关,并与CIK细胞作用的时间关系密切.
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