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目的研究醋酸铅对大鼠脑组织神经生长凶子(BDNF)及其受体P75NIR的影响。方法将雌雄各半的健康成年SD大鼠48只随机分为1个对照组和3个染铅组,每组12只。染铅组分别用25、50、100 mg/kg的醋酸铅处理SD大鼠,腹腔注射5 d,于第6天取材,用石墨炉原子吸收法测定大鼠血清和脑组织中的铅含量;逆转录聚合酶链反应(RT-PCR)和免疫组化方法测定脑组织中BDNF mRNA和蛋白的表达;免疫组化测定脑组织中P75NIR的表达。结果大鼠血清和脑组织中铅含量迅速增加,与对照组比较,差异有统计学意义(P<0．01,P<0．05);RT-PCR结果表明,50、100 mg/kg剂量组BDNF mRNA表达在皮层(0．72±0．09,0．77±0．05)与海马组织(0．77±0．10,0．92±0．08)中明显增加,与对照组(0．52±0．05,0．33±0．03)比较,差异有统计学意义(P<0．05);免疫组化分析表明,各剂量组皮层组织BDNF面密度明显增高,平均灰度明显低于对照组,海马部位与对照组比较,各剂量组BDNF面密度明显增加,差异均有统计学意义(P<0．01),50、100 mg/kg组且平均灰度明显下降,与对照组的差异有统计学意义(P<0．01);对照组和25mg/kg组未见P75NIR阳性表达,50、100mg/kg组可见P75NIR阳性表达。结论醋酸铅可以诱导大鼠大脑皮层、海马组织中BDNF和P75NIR的表达,该诱导作用可能在其神经损伤修复中有重要意义。
Objective To study the effects of lead acetate on neuronal growth hormone (BDNF) and its receptor P75NIR in rat brain. Methods 48 healthy adult male and female SD rats were randomly divided into 1 control group and 3 lead-exposed groups, 12 in each group. Lead-exposed rats were treated with 25, 50, 100 mg / kg of lead acetate, respectively. The rats were injected intraperitoneally for 5 days and drawn on the 6th day. The content of lead in serum and brain of rats were determined by graphite furnace atomic absorption spectrometry The expression of BDNF mRNA and protein in brain was measured by Polymerase Chain Reaction (RT-PCR) and immunohistochemistry. The expression of P75NIR in brain tissue was detected by immunohistochemistry. Results The levels of lead in serum and brain tissue of rats increased rapidly with a significant difference compared with the control group (P <0.01, P <0.05). The results of RT-PCR showed that the doses of 50 and 100 mg / kg BDNF mRNA expression was significantly increased in the cortex (0.72 ± 0.09,0.77 ± 0.05) and hippocampus (0.77 ± 0.10,0.92 ± 0.08) compared with the control group (0.52 ± 0.05,0.33 ± 0.03), the difference was statistically significant (P <0.05). Immunohistochemical analysis showed that the surface density of BDNF in each group was significantly increased Compared with the control group, the gray level of BDNF in the hippocampus of each dose group was significantly lower than that of the control group (P <0.01), and the average gray level of 50 and 100 mg / kg group was significantly higher (P <0.01). No positive expression of P75NIR was detected in the control group and 25mg / kg group, but P75NIR expression was observed in 50,100mg / kg group. Conclusion Lead acetate can induce the expression of BDNF and P75NIR in rat cerebral cortex and hippocampus. The induction may be of great significance in the repair of nerve injury.