氯胺酮长期滥用后小鼠海马区caspase-3和PSD-95的表达变化  被引量:2

Change of Caspase-3 and PSD-95 Expression in Hippocampus of Mice with Chronic Ketamine Addiction

在线阅读下载全文

作  者:杜傲 任鹏[1,2] 何柏林[1] 杨顺成 丁润涛[1] 沈瑞鹏[1] 李延柠[1] 董志斌[1] 卢岩[4] 吴旭[1] 

机构地区:[1]中国医科大学法医学院法医病理学教研室,沈阳110122 [2]中国刑警学院法医学系,沈阳110035 [3]沈阳市公安司法鉴定中心,沈阳110003 [4]中国医科大学附属盛京医院卫生部小儿先天畸形重点实验室,沈阳110004

出  处:《中国医科大学学报》2017年第3期193-196,共4页Journal of China Medical University

基  金:国家自然科学基金(81171032;81100807;81671867);辽宁省教育厅科学研究一般项目(L2014316);辽宁省科学技术基金(2015020514)

摘  要:目的研究氯胺酮长期滥用模型中海马区半胱氨酸蛋白酶(caspase)3和突触后密度蛋白(PSD)95的表达变化。方法每日小鼠腹腔注射氯胺酮(30 mg/kg)、持续3个月建立小鼠氯胺酮长期滥用模型,采用免疫组化及Western blotting检测小鼠氯胺酮长期滥用后caspase-3和PSD-95的表达情况。结果免疫组化结果显示caspase-3表达增强,PSD-95表达减弱。Western blotting结果显示caspase-3活化片段蛋白表达升高,PSD-95蛋白表达下降。结论氯胺酮长期滥用致小鼠脑海马区caspase-3表达增加、PSD-95表达减弱,这一结果揭示了长期滥用氯胺酮所致神经毒性作用的可能机制。Objective To study the changes of hippocampal caspase-3 and PSD-95 expression levels in the mice exposed to ketamine 30mg(/kg·d)for three months. Methods Forty C57BL/6 mice were randomly divided into two groups,and the chronic ketamine addiction model was established by giving mice a three month course of daily intraperitoneal injections of ketamine. Immunohistochemical study and Western blotting were applied to observe the expression of caspase-3 and PSD-95 protein. Results There were more expression of caspase-3 and less of PSD-95 in ketamine group as detected by immuohistochemistry. Western blotting results showed caspase-3 active fragment level significantly increased compared to saline group,but PSD-95 protein level was decreased. Conclusion The increased level of caspase-3 protein and reduced expression of PSD-95 are observed after long-term ketamine administration. These findings may provide an evidence for the neurotoxicity in mouse hippocampus of chronic ketamine addition as a recreational drug.

关 键 词:氯胺酮 半胱氨酸蛋白酶3 突触后密度蛋白95 海马 

分 类 号:R89[医药卫生—法医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象