摘要
目的:研究大鼠脑缺血再灌注后腺病毒表达谷氨酸受体羧基肽段对海马CA1区神经元的保护和Bcl-2磷酸化及与Bax结合的影响。方法:将SD大鼠随机分为假手术组、缺血再灌注对照组、表达病毒组、非表达病毒组及溶剂组。采用焦油紫染色、免疫沉淀和免疫印迹检测大鼠缺血再灌注后海马神经元损伤、脑组织Bcl-2的磷酸化及与Bax结合情况。结果:表达病毒组与缺血再灌注对照组、非表达病毒组及溶剂组相比海马CA1区神经元损伤明显减轻,脑组织中Bcl-2磷酸化明显降低,Bcl-2/Bax的结合明显升高(P<0.05)。结论:腺病毒表达谷氨酸受体羧基肽段可能通过降低脑组织中Bcl-2的磷酸化从而增加Bcl-2/Bax的结合,进而对海马CA1区神经元起保护作用。
Objective To study the effects of adenovirus expressing glutamic acid receptor c-terminal peptide paragraph on neuron,phosphorylation of Bcl-2 and the combination of Bcl-2 with Bax in hippocampal CA1 region of rats with brain ischemia and reperfusion. Methods SD rats were randomly divided into 5 groups:sham-operation group (group A),cerebral ischemia and reperfusion group (group B),cerebral ischemia and reperfusion+ expressing virus treatment group (group C),cerebral ischemia and reperfusion + no-expressing virus treatment group (group D) and reperfusion+solvent (group E). Brain injury in hippocampus of rats and change of phosphorylation of Bcl-2 and its combination with Bax was detected by Cresly Violet-strained or Immunoblot assay. Results As compared with those in group B,D,E,the injury in hippocampus CA1 region and phosphorylation of Bcl-2 were significantly decreased,while the combination of Bcl-2 with Bax was increased in group C (P 0.05). Conclusions Adenovirus expressing glutamic acid receptor c-terminal peptide can protect the neurons in hippocampus from ischemia by decreasing phosphorylation of Bcl-2 and increasing the combination of Bcl-2 with Bax.
出处
《实用医学杂志》
CAS
北大核心
2010年第23期4303-4305,共3页
The Journal of Practical Medicine
基金
国家自然科学基金资助项目(编号:30800309
30800446)
江苏省自然科学基金项目(编号:BK2006536
BK2006035)
徐州医学院院长专项基金项目(编号:08KJZ02)
江苏省普通高等学校"青蓝工程"