油茶皂素对枸橼酸致豚鼠咳嗽的影响

Effect of Camellia Saponin on Citrate-induced Cough in Guinea Pig

目的:探讨油茶皂素防治枸橼酸所致豚鼠咳嗽的作用。方法:豚鼠随机分成正常组、模型组、可待因组、油茶皂素高、中、低剂量组(125、75、25 mg·kg-1),分别连续灌胃给药7 d,最后1次给药1 h后,采用枸椽酸致豚鼠咳嗽模型,以生物信息采集系统记录咳嗽信号、录音和人工计数等方法统计咳嗽次数和咳嗽潜伏期,并对支气管进行病理切片观察。结果:与模型组咳嗽次数(51.3±9.7)次相比,油茶皂素高(31.5±8.7)次、中(38.6±8.2)次、低(35.4±3.6)次剂量组显示均能降低枸橼酸所致咳嗽次数(P<0.05);与模型组咳嗽潜伏期(35.7±25.3)s相比,只有高剂量组才延长咳嗽潜伏期(46.2±36.7)s(P<0.05)。支气管病理切片显示油茶皂素能保护黏膜上皮的完整性,明显抑制枸橼酸对黏膜组织结构的破坏,减少黏膜下层的血管充血和炎性细胞浸润。结论:油茶皂素对枸橼酸所致豚鼠有镇咳治疗作用。机制可能与其降低C-纤维受体对枸橼酸刺激敏感性及减少豚鼠支气管黏膜下层的血管充血及炎性细胞浸润有关。

Objective： To explore the effect of Sasanquasaponins on citric acid-induced cough in guinea pig. Methods： guinea pigs were randomly divided into normal group, model group,codeine group, and three Sasanquasaponins groups including high-dose, middle-dose,low-dose group（ 125,75,25 g·kg^-1 ）. Rats were continuously lavaged normal saline, codeine or Sasanquasaponins by ig for 7 d; after the last administration, cough was induced by the citric acid in guinea pigs model; the cough signal was recorded by biological information acquisition system; cough frequency and cough incubation period were recorded by recording and manual counting; and the pathological sections of the bronchus were observed. Resuits ： Compared to the mode/group, the frequency of cough （51.3 ±9.7） of Sasanquasaponins high （ 31.5 ± 8.7 ） , middle（38.6 ± 8.2）, low （35.4 ±3.6） dose group induced by citrate decreased （P 〈 0.05 ）;compared to the incubation period of cough of the model group （ 35.7 ± 25.3 ） s, only high dose group was prolonged cough latency （46.2 ± 36.7 ） s （ P 〈 0.05 ）. Bronchial biopsy showed that Sasanquasaponins could protect epithelial integrity, inhibit citrate from damaging mueosal structure, and reduce the submueosa vascular congestion and inflammatory cell infiltration. Conclusion： The citric acid-induced cough in guinea pig could be prevented and cured by Sasanquasaponins. Mechanism may be related to the decrease of C-fibre receptors of citric acid stimulation sensitivity and the guinea pig bronchial submucosal vascular congestion, and inflammatory cell infiltration.