Nicotine alleviates chronic stress-induced anxiety and depressive-like behavior and hippocampal neuropathology via regulating autophagy signaling

自噬 尼古丁 皮质酮 慢性应激 神经保护 PI3K/AKT/mTOR通路 蛋白激酶B 药理学 活力测定 内分泌学 海马结构 医学 内科学 细胞凋亡 化学 生物化学 激素
作者
Xi Xiao,Xueliang Shang,Baohui Zhai,Hui Zhang,Tao Zhang
出处
期刊:Neurochemistry International [Elsevier BV]
卷期号:114: 58-70 被引量:55
标识
DOI:10.1016/j.neuint.2018.01.004
摘要

Recently, we reported that chronic nicotine significantly improved chronic stress-induced impairments of cognition and the hippocampal synaptic plasticity in mice, however, the underlying mechanism still needs to be explored. In the present study, 32 male C57BL/6 mice were divided into four groups: control (CON), stress (CUS), stress with chronic nicotine administration (CUS + Nic) and chronic nicotine administration (Nic). The anxiety-like behavior and neuropathological alteration of DG neurons were examined. Moreover, PC12 cells were examined with corticosterone in the presence or absence of nicotine. Both cell viability and apoptosis were determined. When treated simultaneously with an unpredictable chronic mild stress (CUS), nicotine (0.2 mg/kg/d) attenuated behavioral deficits and neuropathological alterations of DG neurons. Moreover, Western blotting showed that chronic nicotine also elevated the level of autophagy makers including Beclin-1 and LC3 II triggered by CUS. In addition, concomitant treatment with nicotine (10 μM) significantly attenuated the loss of PC12 cell viability (p < .01) and apoptosis compared to that of corticosterone treatment alone. Besides, chronic nicotine also enhanced the protein and RNA expression levels of autophagy makers triggered by corticosterone, such as Beclin-1, LC3 II and p62/SQSTM1. However, the above improvements were significantly blocked by autophagy inhibitor 3-MA. Importantly, the activation of the PI3K/Akt/mTOR signaling was carefully tested to illuminate the effects of chronic nicotine. Consequently, chronic nicotine played a role of neuroprotection in either CUS mice or corticosterone cells associating with the enhancement of the autophagy signaling, which was involved in activating the PI3K/Akt/mTOR signaling.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
打打应助张天采纳,获得30
2秒前
CaoRouLi发布了新的文献求助10
2秒前
zhaozhaozhao完成签到,获得积分10
2秒前
CYY发布了新的文献求助10
5秒前
6秒前
朱建军应助隐形书白采纳,获得10
8秒前
8秒前
必过六级应助英勇的白风采纳,获得20
8秒前
song发布了新的文献求助10
9秒前
11秒前
桐桐应助开心的勇敢采纳,获得100
12秒前
Akim应助微眠采纳,获得10
12秒前
13秒前
刘浩营发布了新的文献求助10
15秒前
16秒前
隐形曼青应助官官采纳,获得10
16秒前
16秒前
19秒前
搜集达人应助hyue采纳,获得10
21秒前
田様应助CaoRouLi采纳,获得10
22秒前
chen完成签到,获得积分10
22秒前
22秒前
舍予有服发布了新的文献求助10
24秒前
demmeretock完成签到,获得积分10
25秒前
25秒前
CodeCraft应助yzn采纳,获得10
26秒前
29秒前
33秒前
微眠发布了新的文献求助10
33秒前
yzn完成签到,获得积分10
34秒前
35秒前
咩咩羊完成签到,获得积分10
36秒前
小老头儿完成签到,获得积分10
38秒前
40秒前
Xiaojie发布了新的文献求助10
40秒前
量子星尘发布了新的文献求助10
41秒前
阳光冰颜完成签到 ,获得积分10
41秒前
41秒前
42秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3988975
求助须知:如何正确求助?哪些是违规求助? 3531316
关于积分的说明 11253424
捐赠科研通 3269917
什么是DOI,文献DOI怎么找? 1804830
邀请新用户注册赠送积分活动 882063
科研通“疑难数据库(出版商)”最低求助积分说明 809068