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张尤新, 叶丽平, 包翠芬, 赵艳. 急性染铅对大鼠海马Ca2+-CaMKⅡ信号通路影响[J]. 中国公共卫生, 2010, 26(9): 1154-1155. DOI: 10.11847/zgggws2010-26-09-36
引用本文: 张尤新, 叶丽平, 包翠芬, 赵艳. 急性染铅对大鼠海马Ca2+-CaMKⅡ信号通路影响[J]. 中国公共卫生, 2010, 26(9): 1154-1155. DOI: 10.11847/zgggws2010-26-09-36
ZHANG You-xin, YE Li-ping, BAO Cui-fen, . Effect of acute lead exposure on Ca2+-CamkⅡ signal in hippocampus in rats[J]. Chinese Journal of Public Health, 2010, 26(9): 1154-1155. DOI: 10.11847/zgggws2010-26-09-36
Citation: ZHANG You-xin, YE Li-ping, BAO Cui-fen, . Effect of acute lead exposure on Ca2+-CamkⅡ signal in hippocampus in rats[J]. Chinese Journal of Public Health, 2010, 26(9): 1154-1155. DOI: 10.11847/zgggws2010-26-09-36

急性染铅对大鼠海马Ca2+-CaMKⅡ信号通路影响

Effect of acute lead exposure on Ca2+-CamkⅡ signal in hippocampus in rats

  • 摘要: 目的 探讨急性染铅对大鼠海马Ca2+-Ca2+/钙调蛋白依赖蛋白激酶Ⅱ(CaMKⅡ)信号转导通路影响及作用机制.方法 取30 d健康大鼠海马脑片分别用含醋酸铅(20μmol/L)及不含醋酸铅的人工脑脊液(ACSF)孵育,分对照组、谷氨酸组、CaMKⅡ抑制剂(KN-93)组、谷氨酸+醋酸铅组,培养30 min后收集脑片,用Western Blot方法检测谷氨酸组、KN-93组、铅组中环腺苷酸(cAMP)反应元件结合蛋白(CREB)的活性.结果 染铅组于染铅0、120min时CREB活性分别为(0.305 6±0.020 8)和(0.172 2±0.023 3),随染铅时间延长明显降低;谷氨酸使磷酸化CREB活性提高47%,对非磷酸化CREB活性无影响;KN-93及谷氨酸+醋酸铅组CREB活性分别下降20%,45%,总量CREB表达无明显改变.结论 急性铅中毒可能通过抑制CaMKⅡ活性影响下游信号分子,造成对学习记忆功能的损伤.

     

    Abstract: Objective To study the effect of acute lead exposure on Ca2+-CamkⅡ signal in rat hippo campus.Methods Hippocam palslices of 30 day sold heathy rat were collected and incubated with lead acetate(20 μmol/L)and non lead ace tate in artificial cerebro spinal fluid(ACSF)for the control,glutam ate,CaM KⅡ inhibitor(KN-93),and glutamic acid + lead ace tate group.Brain slices were collected after 30 min of culture.Western Blot was adopted to detect the activity of cyclic adeno sine-3'-5' mono phosphate response element binding prote in(CREB).Results CREB activity in the lead groupdecrea sed significantly with the time of lead exposure.CREB activity increa sed by 47% in glutam ate group and decreased by 20%,45% in KN-93 and glutamic acid+ lead acetate groups.There was no significant change in total CREB expression.Conclusion A cute lead poisoning may inhibit the activity of Ca MKⅡ and affect the downstream signaling molecules resulting in learning and memory damage.

     

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