摘要
目的探讨神经调节素1β(NRG1β)对实验性老年痴呆大鼠神经元凋亡及Bcl-2和Bax表达的影响。方法成年健康雄性Wistar大鼠30只,随机分为假手术组、模型组、治疗组各10只,经左侧脑室微量注射淀粉样蛋白β1-40(Aβ1-40)建立实验性痴呆模型,经右侧脑室注射NRG1β干预治疗,Y型电迷宫检测大鼠的认知功能,原位缺口末端标记法(TUNEL)检测神经细胞凋亡,免疫组织化学法检测Bcl-2和Bax表达。结果造模成功后,模型组大鼠较对照组认知能力明显下降,TUNEL阳性细胞数明显增多,神经细胞Bcl-2和Bax蛋白表达增强(P<0.05)。经NRG1β治疗后,治疗组大鼠较模型组认知能力显著改善,TUNEL阳性细胞显著减少,Bcl-2表达增强,Bax表达减弱(P<0.05)。结论 NRG1β可能通过调节Bcl-2和Bax表达而抑制神经细胞凋亡,从而改善实验性痴呆大鼠学习记忆能力。
Objective To investigate the effect of neuregulin 1β （NRG1β） on the neuronal apoptosis and the expressions of Bcl-2 and Bax in experimental dementia model rats. Methods Thirty adult healthy male Wistar rats were randomly divided into control group, model group and treated group consisting of 10 rats respectively. The experimental dementia models were established by injecting beta-amyloid protein 1-40 （Aβ1-40 ） stereotactically into the left lateral ventricle, and treated by injecting NRGl13 into right lateral ventricle. The cognitive capacity of rats was evaluated with Yelectric maze. The neuronal apoptosis was counted by terminal deoxynueleotidyl transferase mediated dUTP nick end labeling（TUNEL） assay. The expressions of Bcl-2 and Bax were determined with immunohistochemistry assay. Results The cognitive ability in model group rats decreased, along with the number of neuronal apoptosis and the expressions of Bcl-2 and Bax increased significantly than those in control group （P 〈 0. 05）. After treatment with NRG1β, the cognitive ability of rats improved, the number of neuronal apoptosis reduced and the expression of Bcl-2 increased while Bax decreased significantly than those in model group （ P 〈 0.05 ）. Conclusion NRG1β could inhibit neuronal apoptosis by regulating the expressions of Bcl-2 / Bax to improve the capacity of learning and memory in experimental dementia rats.
出处
《解剖学报》
CAS
CSCD
北大核心
2010年第5期666-669,共4页
Acta Anatomica Sinica
基金
山东省自然科学(博士)基金项目(2008BS02026)资助
