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本文引用的文献

1
[Research advances in association between pediatric obesity and bronchial asthma].[儿童肥胖与支气管哮喘相关性的研究进展]
Zhongguo Dang Dai Er Ke Za Zhi. 2016 Jul;18(7):671-6. doi: 10.7499/j.issn.1008-8830.2016.07.020.
2
Role of the ion channel, transient receptor potential cation channel subfamily V member 1 (TRPV1), in allergic asthma.离子通道,即瞬时受体电位阳离子通道亚家族V成员1(TRPV1),在过敏性哮喘中的作用。
Respir Res. 2016 Jun 2;17(1):67. doi: 10.1186/s12931-016-0384-x.
3
Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation.沉默伤害感受器神经元可减轻过敏性气道炎症。
Neuron. 2015 Jul 15;87(2):341-54. doi: 10.1016/j.neuron.2015.06.007. Epub 2015 Jun 25.
4
Increased expression of bronchial epithelial transient receptor potential vanilloid 1 channels in patients with severe asthma.在严重哮喘患者的支气管上皮细胞中,瞬时受体电位香草素 1 通道的表达增加。
J Allergy Clin Immunol. 2014 Mar;133(3):704-12.e4. doi: 10.1016/j.jaci.2013.09.016. Epub 2013 Nov 8.
5
Rise of the sensors: nociception and pruritus.传感器的兴起:痛觉和瘙痒。
Curr Allergy Asthma Rep. 2012 Apr;12(2):104-14. doi: 10.1007/s11882-012-0245-8.
6
Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers.通过TRPV1介导的非渗透性钠通道阻滞剂的进入来抑制伤害感受器。
Nature. 2007 Oct 4;449(7162):607-10. doi: 10.1038/nature06191.
7
Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons.饮食诱导的肥胖会在弓状黑皮质素神经元中引起严重但可逆的瘦素抵抗。
Cell Metab. 2007 Mar;5(3):181-94. doi: 10.1016/j.cmet.2007.02.004.
8
Obesity, smooth muscle, and airway hyperresponsiveness.肥胖、平滑肌与气道高反应性。
J Allergy Clin Immunol. 2005 May;115(5):925-7. doi: 10.1016/j.jaci.2005.01.064.
9
The high-fat diet-fed mouse: a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes.高脂饮食喂养的小鼠:一种用于研究糖耐量受损和2型糖尿病机制及治疗方法的模型。
Diabetes. 2004 Dec;53 Suppl 3:S215-9. doi: 10.2337/diabetes.53.suppl_3.s215.
10
Nerve growth factor levels and localisation in human asthmatic bronchi.人哮喘支气管中神经生长因子的水平及定位
Eur Respir J. 2002 Nov;20(5):1110-6. doi: 10.1183/09031936.02.00205402.

[高脂饮食对小鼠呼吸道和背根神经节中瞬时受体电位香草酸亚型1表达的影响]

[Effect of high-fat diet on expression of transient receptor potential vanilloid 1 in respiratory tract and dorsal root ganglion of mice].

作者信息

Zhu Lian, Xu Zhi-Liang

机构信息

Department of Pediatrics, Renmin Hospital of Wuhan University, Wuhan 430060, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2017 Jul;19(7):826-831. doi: 10.7499/j.issn.1008-8830.2017.07.019.

DOI:10.7499/j.issn.1008-8830.2017.07.019
PMID:28697840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7389912/
Abstract

OBJECTIVE

To investigate the effect of high-fat diet on the expression of transient receptor potential vanilloid 1 (TRPV1) in the respiratory system and the dorsal root ganglion (DRG) of mice, as well as its effect on the excitability of sensory neurons.

METHODS

A total of 20 C57BL/6 mice were randomly divided into normal-diet (ND) group and high-fat diet (HFD) group, with 10 mice in each group. The mice were given corresponding diets and body weights were monitored. After 7 weeks of feeding, lung tissue, bronchial tissue, and DRG at thoracic segments 3-4 were collected and immunohistochemical staining was performed. A patch clamp was used to measure the number of action potentials and TRPV1 current intensity in the DRG.

RESULTS

After 7 weeks of feeding, the HFD group had significantly greater mean weight gain than the ND group (6.4±2.6 g vs 2.3±0.5 g; P<0.001). The HFD group had significantly higher expression of TRPV1 in the bronchus, pulmonary alveoli, and DRG than the ND group (P<0.05). Compared with the ND group, the HFD group had significant increases in the TRPV1 current intensity and number of action potentials in the DRG (P<0.05).

CONCLUSIONS

High-fat diet induces a significant increase in body weight and leads to high expression of TRPV1 and high excitability in the respiratory system and the peripheral sensory neurons. This suggests that TRPV1 may be an important factor in the physiopathological mechanisms of bronchial hyperresponsiveness.

摘要

目的

探讨高脂饮食对小鼠呼吸系统及背根神经节(DRG)中瞬时受体电位香草酸亚型1(TRPV1)表达的影响,及其对感觉神经元兴奋性的影响。

方法

将20只C57BL/6小鼠随机分为正常饮食(ND)组和高脂饮食(HFD)组,每组10只。给予小鼠相应饮食并监测体重。喂养7周后,收集肺组织、支气管组织及胸段3 - 4的DRG,进行免疫组织化学染色。采用膜片钳技术测量DRG中动作电位的数量和TRPV1电流强度。

结果

喂养7周后,HFD组的平均体重增加显著高于ND组(6.4±2.6 g对2.3±0.5 g;P<0.001)。HFD组支气管、肺泡及DRG中TRPV1的表达显著高于ND组(P<0.05)。与ND组相比,HFD组DRG中TRPV1电流强度和动作电位数量显著增加(P<0.05)。

结论

高脂饮食导致体重显著增加,并使呼吸系统和外周感觉神经元中TRPV1高表达且兴奋性增强。这表明TRPV1可能是支气管高反应性生理病理机制中的一个重要因素。