摘要
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 study the role of CamkⅡ in acute lead exposure of rat hippocampus.Methods The hippocampus of 30 day healthy Wistar rat was taken out quickly and cut into 350 μm slices.After stabilizing culture for 2 hours in artificial cerebrospinal fluid（ACSF）,the slices were diveded into control（ACSF）group,glutamic acid group,KN-93（CaMKⅡinhibitor）group and glutamic acid ＋ lead group.After 30 min culture,the hippocampus slices were collected to detect effects of glutamic acid,KN-93 and lead on extracellular signal regulated kinase2（ERK2）.Results Compared with the control group,there was a 42% inerease of ERK2 activcty with a significant difference（P0.05） in glutamic acid guoup.There were a 23% and a 28% decrease of ERK2 activity in KN-93 and lead exposure guoups compared with that of control guoup（P〈0.05）.Total ERK2 expression was not affected obviously.Conclusion Actue lead exposure inhibits CaMKⅡ activity and affects its downstream signal resulting in nervous system impairment.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2009年第12期1524-1525,共2页
Chinese Journal of Public Health
基金
国家自然科学基金(39970651)
