College of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, 210046, China.
College of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, 210046, China.
J Ethnopharmacol. 2019 May 23;236:82-90. doi: 10.1016/j.jep.2019.02.043. Epub 2019 Mar 2.
San'ao decoction (SAD), a traditional Chinese prescription, is well-known in asthma treatment. In the current study, the protective role of SAD and its mechanism in aggravated asthma mice model via regulation of TRP channel were evaluated and explored.
UPLC-QTOF-MS was used for analyzing the chemicals in SAD. The major chemical components in SAD were separated and detected under an optimized chromatographic and MS condition. 75 BALB/c mice were randomly divided into five groups: normal group, model group, dexamethasone group (0.75 mg kg), SAD-high dose group (1.8 g kg) and SAD-low dose group (0.9 g kg). A 42 days aggravated asthmatic model was established in mice induced by ovalbumin (OVA) plus PM2.5 (1.6 mg kg). After treated with corresponding medicine, peripheral blood and bronchoalveolar lavage fluid (BALF) from each group were assessed, airway responsiveness was determined, histopathological changes in lungs were detected, relevant cytokines and neurokines levels were measured, TRPA1 and TRPV1 mRNA and protein expressions in lung tissues were examined as well.
21 signal peaks of the chemicals in SAD were identified with the method of UPLC-QTOF-MS. SAD, especially SAD-high dose exerted significant effects on OVA plus PM2.5 mice model in relieving lung injury score (P < 0.05), reducing eosinophil (EOS) count in blood (P < 0.05) and inflammatory cells ratio in BALF (P < 0.05, P < 0.01), decreasing RI value (P < 0.05) while increasing Cdyn value (P < 0.05), reducing IL-13, PGD and NGF levels in BALF (P < 0.01), as well as down-regulating TRPA1 and TRPV1 mRNA and protein expressions in lung tissues (P < 0.05, P < 0.01).
SAD could improve pulmonary functions, relieve lung injury, as well as reduce IL-13, PGD and NGF levels of OVA plus PM2.5 aggravated asthma model in mice. The effect and mechanism of SAD might be related to the inhibition of TRPA1 and TRPV1 channels.
三拗汤（SAD）是一种传统的中药方剂，在哮喘治疗中广为人知。本研究旨在通过调节瞬时受体电位香草酸亚型 1（TRPA1）和瞬时受体电位阳离子通道亚家族 V 型 1（TRPV1）通道评估 SAD 对加重型哮喘小鼠模型的保护作用及其机制。
采用超高效液相色谱-四极杆飞行时间质谱联用（UPLC-QTOF-MS）分析 SAD 中的化学成分。在优化的色谱和 MS 条件下，分离和检测 SAD 中的主要化学成分。将 75 只 BALB/c 小鼠随机分为 5 组：正常组、模型组、地塞米松组（0.75mg/kg）、SAD 高剂量组（1.8g/kg）和 SAD 低剂量组（0.9g/kg）。通过卵清蛋白（OVA）联合 PM2.5（1.6mg/kg）诱导建立 42 天加重型哮喘小鼠模型。用相应的药物处理后，检测各组外周血和支气管肺泡灌洗液（BALF），测定气道反应性，检测肺组织的组织病理学变化，测定相关细胞因子和神经激肽水平，检测肺组织中 TRPA1 和 TRPV1mRNA 和蛋白的表达。
采用 UPLC-QTOF-MS 方法鉴定了 SAD 中 21 种化学成分的信号峰。SAD，特别是 SAD 高剂量组，对 OVA 联合 PM2.5 小鼠模型具有显著的缓解作用，可降低肺损伤评分（P<0.05），降低血液中嗜酸性粒细胞（EOS）计数（P<0.05）和 BALF 中炎症细胞比例（P<0.05，P<0.01），降低 RI 值（P<0.05），增加 Cdyn 值（P<0.05），降低 BALF 中白细胞介素-13（IL-13）、前列腺素 D2（PGD）和神经生长因子（NGF）水平（P<0.01），下调肺组织中 TRPA1 和 TRPV1mRNA 和蛋白的表达（P<0.05，P<0.01）。
SAD 可改善肺功能，减轻 OVA 联合 PM2.5 加重型哮喘模型小鼠的肺损伤，降低 IL-13、PGD 和 NGF 水平。SAD 的作用和机制可能与抑制 TRPA1 和 TRPV1 通道有关。
