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参麦注射液对哮喘大鼠气道平滑肌细胞增殖的影响及作用机制。

The effect of Shenmai injection on the proliferation of Rat airway smooth muscle cells in asthma and underlying mechanism.

机构信息

Department of Respiratory Medicine and Intensive Care Union, Henan Provincial Peoples' Hospital of Zhengzhou University, Zhengzhou 450003, China.

出版信息

BMC Complement Altern Med. 2013 Sep 8;13:221. doi: 10.1186/1472-6882-13-221.

DOI:10.1186/1472-6882-13-221
PMID:24010863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3849921/
Abstract

BACKGROUND

Over-proliferation of airway smooth muscle cell (ASMC) is one of the important contributors to airway remodeling in asthma. The aim of this study was to investigate the effect of Shenmai injection (SMI) on the proliferation of the rat ASMC in asthma.

METHODS

Rats were randomly divided into three groups: the control group, the asthma group, and the SMI treatment group. Reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry staining were used to detect the mRNA and protein expression of transient receptor potential vanilloid 1 (TRPV1) and proliferating cell nuclear antigen (PCNA) in rat ASMC respectively. Intracellular Ca²⁺ concentration ( Ca²⁺) in rat ASMC were measured with Fluo-3/AM by confocal microscopy. The proliferation was detected by MTT assay.

RESULTS

Compared with the control group, the asthma group showed an increased expression of TRPV1 and Ca²⁺ in rat ASMC. The expression of PCNA and absorbance of MTT assay in asthma rat ASMC was also significantly increased. SMI could significantly decrease the expression of TRPV1 channel and Ca²⁺ in the asthmatic rat ASMC. Furthermore, the expression of PCNA and absorbance of MTT assay in asthmatic rat ASMC was significantly reduced after SMI treatment.

CONCLUSIONS

SMI may prevent asthma-induced ASMC over-proliferation probably by inhibiting the expression of TRPV1 channel, which regulates the intracellular calcium concentration.

摘要

背景

气道平滑肌细胞（ASMC）的过度增殖是哮喘气道重塑的重要原因之一。本研究旨在探讨参麦注射液（SMI）对哮喘大鼠 ASMC 增殖的影响。

方法

将大鼠随机分为三组：对照组、哮喘组和 SMI 治疗组。采用逆转录-聚合酶链反应（RT-PCR）和免疫细胞化学染色法分别检测大鼠 ASMC 中转瞬受体电位香草酸 1 型（TRPV1）和增殖细胞核抗原（PCNA）的 mRNA 和蛋白表达。采用共聚焦显微镜用 Fluo-3/AM 测定大鼠 ASMC 内的细胞内 Ca²⁺浓度（[Ca²⁺]（i））。通过 MTT 测定法检测细胞增殖。

结果

与对照组相比，哮喘组大鼠 ASMC 中 TRPV1 的表达和[Ca²⁺]（i）增加。哮喘大鼠 ASMC 中 PCNA 的表达和 MTT 测定的吸光度也显著增加。SMI 可显著降低哮喘大鼠 ASMC 中 TRPV1 通道和[Ca²⁺]（i）的表达。此外，SMI 治疗后哮喘大鼠 ASMC 中 PCNA 的表达和 MTT 测定的吸光度明显降低。

结论

SMI 可能通过抑制 TRPV1 通道的表达来预防哮喘引起的 ASMC 过度增殖，从而调节细胞内 Ca²⁺浓度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/e05a20802b2f/1472-6882-13-221-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/025035a82045/1472-6882-13-221-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/3109de6f4d7e/1472-6882-13-221-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/d850b469d84f/1472-6882-13-221-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/eff2c8bcc68a/1472-6882-13-221-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/735609681b42/1472-6882-13-221-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/e05a20802b2f/1472-6882-13-221-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/025035a82045/1472-6882-13-221-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/3109de6f4d7e/1472-6882-13-221-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/d850b469d84f/1472-6882-13-221-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/eff2c8bcc68a/1472-6882-13-221-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/735609681b42/1472-6882-13-221-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf2/3849921/e05a20802b2f/1472-6882-13-221-6.jpg

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