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神经生长因子诱导背根神经节感觉神经元中诱导型一氧化氮合酶和P物质以及干扰素调节因子-1的表达。

Nerve growth factor induced expression of iNOS and substance P in dorsal root ganglion sensory neuron and interferon regulatory factor-1.

作者信息

Pan Pinhua, Huang Siyun, Hu Chengping

机构信息

Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha 410008, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2011 May;36(5):386-91. doi: 10.3969/j.issn.1672-7347.2011.05.003.

DOI:10.3969/j.issn.1672-7347.2011.05.003
PMID:21685692
Abstract

OBJECTIVE

To investigate the mechanism of airway neurogenic inflammation by studying the expression of inducible nitric oxide synthase (iNOS) and substance P in C(7)-T(5) dorsal root ganglion sensory neuron cells induced by nerve growth factor (NGF) and the role of interferon regulatory factor-1 (IRF-1).

METHODS

The dorsal root ganglia neuron (DRGn) cells were primary cultured, and then stimulated with or without NGF or NGF+interferon (IFN)-γ. Subsequently the DRGn cells were transinfected with or without green fluorescent protein (GFP)-IRF-1-vshRNA, and then stimulated with or without NGF. The expressions of iNOS and substance P were detected by real-time PCR.

RESULTS

NGF induced the mRNA expression of iNOS and substance P in dorsal root ganglion sensory neuron cells, and IFN-γ increased NGF-induced iNOS mRNA expression. The expressions of iNOS and substance P in sensory neuron cells were decreased significantly at the mRNA level after IRF-1 was blocked down by IRF-1-vshRNA transinfection.

CONCLUSION

NGF is involved in the airway neurogenic inflammation by prompting the expression of iNOS and substance P through transcription factor IRF-1 in airway sensory neuron cells. IRF-1 may be a therapeutic target for airway neurogenic inflammation.

摘要

目的

通过研究神经生长因子(NGF)诱导的C(7)-T(5)背根神经节感觉神经元细胞中诱导型一氧化氮合酶(iNOS)和P物质的表达以及干扰素调节因子-1(IRF-1)的作用,探讨气道神经源性炎症的机制。

方法

原代培养背根神经节神经元(DRGn)细胞,然后用或不用NGF或NGF+干扰素(IFN)-γ刺激。随后,用或不用绿色荧光蛋白(GFP)-IRF-1-vshRNA转染DRGn细胞,然后用或不用NGF刺激。通过实时PCR检测iNOS和P物质的表达。

结果

NGF诱导背根神经节感觉神经元细胞中iNOS和P物质的mRNA表达,IFN-γ增加NGF诱导的iNOS mRNA表达。通过IRF-1-vshRNA转染阻断IRF-1后,感觉神经元细胞中iNOS和P物质的mRNA水平显著降低。

结论

NGF通过转录因子IRF-1促进气道感觉神经元细胞中iNOS和P物质的表达,参与气道神经源性炎症。IRF-1可能是气道神经源性炎症的治疗靶点。

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