School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300072, China.
Chin Med J (Engl). 2009 Dec 20;122(24):3020-4.
It has been found that the expression of cystic fibrosis transmembrane conductance regulator (CFTR) is closely related to allergic rhinitis (AR). In the previous study, we have demonstrated that antiallergic herbal agents (AHA) can obviously inhibit the allergic reaction of AR. The aim of this study was to explore the expression of CFTR and the effects of AHA on CFTR to improve the allergic reaction of AR.
An animal model of an AR rabbit was established using ovalbumin (OVA). The rhinitis rabbits were randomly assigned to three groups: AHA treating group (AHATG), modeling group (MG) and healthy controlling group (HCG). The expressions of CFTR protein were examined by immunohistochemical method. The mucosal epithelial cells of all the rabbits were primarily cultured with tissue culture method in vitro and treated with or without glibenclamide for 24 hours. The levels of monocyte chemotactic factor-1 (MCP-1) and RANTES protein in supernatants of culture were measured by ELISA, and the expressions of CFTR mRNA were detected by real-time PCR.
The expressions of CFTR mRNA and protein greatly increased in mucosal epithelial cells of MG. The protein concentrations of MCP-1, RANTES in culture supernatants of MG were significantly higher than those in the other two groups (P < 0.01), and they reached much higher level than those at the start points in the MG (P < 0.05) and were significantly different compared with those in the AHATG after being cultured for 24 hours (P < 0.01). CFTR mRNA in MG + glibenclamide were much lower than those in MG (P < 0.05). RANTES and CFTR mRNA treated with glibenclamide in AHATG were significantly lower than those in the AHATG (P < 0.01). Minimal changes in the secretions of MCP-1 in the epithelial cells were detected between AHATG and AHATG + glibenclamide (P > 0.05).
AHA can inhibit the secretions of CFTR, RANTES and MCP-1 in mucosal epithelia and improve inflammatory reaction of AR. CFTR may play an important role in the secretion of RANTES and mucosal inflammatory response in AR. Glibenclamide can inhibit the CFTR secretion in mucosal epithelial cells, in particular during AR process. These effects of glibenclamide on secretion of RANTES can be effectively strengthened by AHA.
囊性纤维化跨膜电导调节因子（CFTR）的表达与过敏性鼻炎（AR）密切相关。在之前的研究中，我们已经证明抗变态反应草药（AHA）可以明显抑制 AR 的过敏反应。本研究旨在探讨 CFTR 的表达及 AHA 对 CFTR 的作用，以改善 AR 的过敏反应。
采用卵清蛋白（OVA）建立 AR 兔动物模型。将鼻炎兔随机分为三组：AHA 治疗组（AHATG）、模型组（MG）和健康对照组（HCG）。采用免疫组织化学方法检测 CFTR 蛋白的表达。采用组织培养法体外原代培养所有兔的黏膜上皮细胞，分别用或不用格列本脲处理 24 小时。用酶联免疫吸附法（ELISA）检测培养上清液中单核细胞趋化因子-1（MCP-1）和 RANTES 蛋白的水平，实时 PCR 检测 CFTR mRNA 的表达。
MG 组黏膜上皮细胞 CFTR mRNA 和蛋白表达明显增加。MG 组培养上清液中 MCP-1、RANTES 蛋白浓度明显高于其余两组（P < 0.01），且较 MG 组起始点明显升高（P < 0.05），与 MG 组经 24 小时培养后差异有统计学意义（P < 0.01）。MG+格列本脲组 CFTR mRNA 明显低于 MG 组（P < 0.05）。AHATG+格列本脲组 RANTES 和 CFTR mRNA 明显低于 AHATG 组（P < 0.01）。AHATG 组与 AHATG+格列本脲组上皮细胞 MCP-1 分泌变化不明显（P > 0.05）。
AHA 可抑制 AR 黏膜上皮 CFTR、RANTES 和 MCP-1 的分泌，改善 AR 炎症反应。CFTR 可能在 AR 中 RANTES 分泌和黏膜炎症反应中起重要作用。在 AR 过程中，格列本脲可抑制黏膜上皮细胞 CFTR 的分泌。AHA 可有效增强格列本脲对 RANTES 分泌的抑制作用。
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