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CLC number: R587.2

On-line Access: 2020-03-02

Received: 2019-07-19

Revision Accepted: 2019-11-12

Crosschecked: 2020-02-04

Cited: 0

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Citations:  Bibtex RefMan EndNote GB/T7714


Lan Xu


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Journal of Zhejiang University SCIENCE B 2020 Vol.21 No.2 P.166-171


CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord

Author(s):  Cheng-ming Ni, Bing-yu Ling, Xiang Xu, He-ping Sun, Hui Jin, Yu-qiu Zhang, Hong Cao, Lan Xu

Affiliation(s):  Department of Endocrinology, the Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi 214023, China; more

Corresponding email(s):   hongcao@fudan.edu.cn, xulan126@126.com

Key Words:  FKN/CX3CR1, Mechanical allodynia, STZ-induced diabetic mice

Cheng-ming Ni, Bing-yu Ling, Xiang Xu, He-ping Sun, Hui Jin, Yu-qiu Zhang, Hong Cao, Lan Xu. CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord[J]. Journal of Zhejiang University Science B, 2020, 21(2): 166-171.

@article{title="CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord",
author="Cheng-ming Ni, Bing-yu Ling, Xiang Xu, He-ping Sun, Hui Jin, Yu-qiu Zhang, Hong Cao, Lan Xu",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord
%A Cheng-ming Ni
%A Bing-yu Ling
%A Xiang Xu
%A He-ping Sun
%A Hui Jin
%A Yu-qiu Zhang
%A Hong Cao
%A Lan Xu
%J Journal of Zhejiang University SCIENCE B
%V 21
%N 2
%P 166-171
%@ 1673-1581
%D 2020
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1900439

T1 - CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord
A1 - Cheng-ming Ni
A1 - Bing-yu Ling
A1 - Xiang Xu
A1 - He-ping Sun
A1 - Hui Jin
A1 - Yu-qiu Zhang
A1 - Hong Cao
A1 - Lan Xu
J0 - Journal of Zhejiang University Science B
VL - 21
IS - 2
SP - 166
EP - 171
%@ 1673-1581
Y1 - 2020
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1900439

Patients with diabetic peripheral neuropathy experience debilitating pain that significantly affects their quality of life (Abbott et al., 2011), by causing sleeping disorders, anxiety, and depression (Dermanovic Dobrota et al., 2014). The primary clinical manifestation of painful diabetic neuropathy (PDN) is mechanical hypersensitivity, also known as mechanical allodynia (MA) (Callaghan et al., 2012). MA’s underlying mechanism remains poorly understood, and so far, based on symptomatic treatment, it has no effective therapy (Moore et al., 2014).


方法:本实验采用健康雄性C57BL/6小鼠与CX3CR1 KO小鼠,体重20~23 g,隔夜禁食12 h(20点至次日8点),并连续三天腹腔注射100 mg/kg的STZ制备T1DM模型.以空腹血糖浓度>11.1 mmol/L且三周后小鼠机械痛阈值明显下降的情况视为T1DM模型制备成功.在小鼠机械痛阈下降的对应时间点,取腰段脊髓背角,采用蛋白质印迹法(western blot)和免疫组化法测定CX3CL1及CX3CR1的表达情况.同时,在发生机械痛阈值下降的第三周时间鞘内给予CX3CR1的中和抗体,进行机械刺激并观察其痛阈值的变化.
结论:STZ诱导的T1DM动物模型在早期表现为显著的机械诱发痛,并伴随脊髓背角CX3CL1/CX3CR1表达上调;在痛阈下降期鞘内给予CX3CR1的中和抗体可抑制糖尿病小鼠的痛行为.与腹腔注射STZ形成T1DM的C57BL/6小鼠相比,CX3CR1 基因敲除的糖尿病小鼠机械痛阈值下降的时间延迟,程度减轻.因此,我们推测CX3CL1/ CX3CR1可能参与T1DM机械痛的形成与发展.


Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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