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目的探讨Ca2+/钙调蛋白依赖的蛋白激酶Ⅱ(CaMKⅡ)在大鼠海马急性铅中毒的作用机制。方法正常30 d大鼠,取海马制成350μm脑片,人工脑脊液(ACSF)液中稳定培养2 h后,分为4组,对照组(仍为普通ACSF液)、谷氨酸组、KN-93(CaMKⅡ抑制剂)组、谷氨酸加醋酸铅组。培养30 min后收集脑片,用蛋白免疫印迹(Westernblot)法检测谷氨酸、抑制剂KN-93和铅对下游信号分子细胞外信号调节激酶2(ERK2)的活性及总量表达的影响。结果大鼠海马脑片培养中,谷氨酸能提高ERK2活性,与对照组比较增加42%,差异有统计学意义(P<0.05)。KN-93及铅能抑制ERK2活性,与对照组比较降低23%,28%,差异有统计学意义(P<0.05)。对总量ERK2表达无明显影响。结论急性铅中毒可能通过抑制CaMKⅡ活性影响下游信号分子,造成神经系统损伤。
Objective To investigate the mechanism of Ca2 + / calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) in acute lead poisoning in hippocampus of rats. Methods The rats in normal group were given 350μm slices of hippocampus and ACSF solution for 2 hours. They were divided into 4 groups: control group (still ACSF), glutamate group, KN- 93 (CaMKⅡ inhibitor) group, glutamate plus lead acetate group. The brain slices were harvested after 30 min. The effects of glutamate, inhibitor of KN-93 and lead on the activity and total expression of downstream signal molecule extracellular signal-regulated kinase 2 (ERK2) were detected by Western blotting. Results Glutamic acid increased ERK2 activity in hippocampal slices of rats compared with the control group, an increase of 42%, the difference was statistically significant (P <0.05). KN-93 and lead inhibited the activity of ERK2, with a 23% and 28% decrease compared with the control group, the difference was statistically significant (P <0.05). No significant effect on the total ERK2 expression. Conclusion Acute lead poisoning may affect downstream signaling molecules by inhibiting the activity of CaMKⅡ, resulting in nervous system injury.