TrkB、TrkB mRNA在新生豚鼠胆红素脑病时的表达

A study on expression of TrkB and TrkB mRNA in bilirubininduced encephalopathy of newborn guinea pig

目的通过实验观察胆红素脑病时脑源性神经营养因子的特异性受体酪氨酸激酶B及酪氨酸激酶B信使RNA在大脑皮层及海马的表达,探讨其在胆红素脑病中可能的作用及机制,为新生儿胆红素脑病新的治疗途径提供实验依据。方法应用免疫组化、原位杂交技术进行实验研究,镜下计数大脑皮层及海马区酪氨酸激酶B、酪氨酸激酶B信使RNA阳性神经元细胞数、阳性神经元细胞平均灰度。结果实验组较对照组酪氨酸激酶B表达增高,注射胆红素8小时后明显增高(P<0.01),且高剂量组比低剂量组增高明显(P<0.05);与对照组相比,注射胆红素后酪氨酸激酶B信使RNA的表达4小时组、8小时组呈持续增加(P<0.01),且8小时组酪氨酸激酶B信使RNA表达高于4小时组(P<0.05)。结论胆红素脑病时,酪氨酸激酶B、酪氨酸激酶B信使RNA随损伤时间的延长和程度的加重而表达增加,提示酪氨酸激酶B的升高对胆红素脑病可能有一定的保护作用。

Objeatve To investigate expression of brain-derived neurotrophic factor （BDNF） TrkB and TrkB mRNA in cerebral cortex and hippocampus in bilirubin-induced encephalopathy by establishing an experimental model and to explore their roles and mechanism of action so as to provide a new approach for treatment of the disease. Methods lmmunohistochemistry and in situ hybridization techniques were used in our experiment. The number of positive-expression neurons was counted and the average grey level of the positive expression neurons was measured in cerebral cortex and hippocampus （the higher the grey level value, the weaker the positive expression intensity）. One-way analysis of variance（ANOVA） was used for inter-group comparison. If the variance between the groups was equal, SNK（ q test） test was used, and ff the variance was unequal, Games-Howell method was adopted. P 〈 O. 05 was regarded as significance test criteria. Results As compared with the control group, expression of TrkB in the experimental group increased, and after 8 hrs. of bilirubin injection, expression of TrkB increased significantly （ P 〈 0.01 ） , and increment in expression of TrkB in high dose of bilirubin injection subgroup was greater than that in the low dose subgroup. Compared with the control group, the expression of TrkB mRNA in the experimental group after 4 hrs. and 8 hrs. of bilirubin injection increased contineously, and that at 8 hrs. was higher than that at 4 hrs. of bilirubin injection. Conclusion In kernicterus, the expression of TrkB and TrkB mRNA increases with the lasting of time and aggravation of injury, indicating that TrkB may protect nerve cells to some extent.