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蛋白激酶B/ 叉头型转录因子O 亚型通路 在腹侧海马损伤大鼠中的作用
白渊翰曾志文
0
()
摘要:
目的 建立精神分裂症的腹侧海马损伤大鼠模型,并探讨模型大脑中蛋白激酶B(PKB/ Akt)和叉头型转录因子O 亚型(FoxOs)蛋白磷酸化活性水平。方法 健康雄性SD 乳鼠随机分为2 组,腹 侧海马损伤组(NVHL)和对照组,每组各8 只大鼠,利用脑立体定位技术注射鹅膏蕈氨酸制备腹侧海马 损伤模型。第56~60 天时,大鼠接受自发活动、前脉冲抑制(PPI)等行为学测试。测试完成3 d 后取大 鼠脑组织进行形态学观察。采用Western blot 测定大鼠皮层和纹状体Akt/FoxOs磷酸化水平。结果 与 对照组大鼠相比,NVHL大鼠腹侧海马明显损伤。安非他命诱导的自发探索活动增加[(1 014±72)次 比(753±87)次,P < 0.01],PPI 受损[PP6:(5.04±3.24)% 比(22.08±14.26)%,PP9:(11.26±5.24)% 比 (25.16±13.45)%,PP12:(8.17±10.45)% 比(29.16±10.25)%,均P < 0.01]。大脑皮层Akt/FoxO1 和纹状 体Akt/FoxO1/FoxO3a磷酸化水平降低( P<0.05)。结论 腹侧海马损伤是一个广泛应用的精神分裂症 动物模型,海马损伤后大鼠皮层和纹状体Akt/FoxOs蛋白磷酸化水平下降,提示该通路参与了精神分裂 症的过程。
关键词:  精神分裂症  海马损伤模型  蛋白激酶B  叉头型转录因子O 亚型
DOI:10.3969/j.issn.1009-6574.2020.11.002
基金项目:国家自然科学基金项目(81701315);广东省自然科学基金项目(2017A030313769); 广东省高水平临床重点专科(深圳市配套建设经费)资助项目(SZGSP013);深圳市科技计划项目 (JCYJ20170306154944261);深圳市“医疗卫生三名工程”项目(SZSM201612006);深圳市医学重点学科 建设经费资助项目(SZXK043)
Role of Akt/FoxOs signaling pathway in ventral hippocampal lesion in rats
Bai Yuanhan, Zeng Zhiwen
()
Abstract:
Objective To establish a rat model of hippocampal injury in schizophrenia, and to investigate the protein phosphorylation activity of protein kinase B( PKB/Akt) and forkhead box Os( FoxOs) protein in the model brain. Methods Healthy male Sprague-Dawley rats were randomly divided into two groups: the neonatal ventral hippocampus lesion( NVHL) and the control group, with 8 rats in each group. The model of NVHL was established by stereotactic injection with ibotenic acid. At 56-60 days, the rats were subjected to spontaneous activity, pre pulse inhibition( PPI) and other behavioral tests. Three days after the test, the brain tissue was taken for morphological observation. Akt/FoxOs phosphorylation levels in cortex and striatum were measured by Western blot. Rusults Compared with the control group, the ventral hippocampus of NVHL rats was significantly damaged. Amphetamine induced spontaneous exploration activity increased [(1 014±72) times vs.( 753±87) times, P < 0.01], PPI was impaired[ PP6:( 5.04±3.24)% vs. (22.08±14.26)%, PP9:( 11.26±5.24)% vs.( 25.16±13.45)%, PP12:( 8.17±10.45)% vs.( 29.16±10.25)%, all P< 0.01] in the NVHL group. The phosphorylation levels of Akt/FoxO1 in cerebral cortex and Akt/FoxO1/ FOXO3a in striatum were decreased( P < 0.05). Conclusions Ventral hippocampal injury is a widely used animal model of schizophrenia. After hippocampal injury, Akt/FoxOs protein phosphorylation levels in cortex and striatum of rats decreased, which further indicated that this pathway was involved in the process of schizophrenia.
Key words:  Schizophrenia  Neonatal ventral hippocampal lesion model  Protein kinase B( PKB/ Akt)  Forkhead Box Os( FoxOs)

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