1.石河子大学药学院/新疆植物药资源利用教育部重点实验室/红花产业研究院,新疆 石河子 832002
2.哈尔滨医科大学药学院,哈尔滨 150081
Received:12 November 2025,
Revised:2026-02-11,
Accepted:12 February 2026,
Published:15 March 2026
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金家成,陈雯艳,李欣,等.基于转录组学的七味冬青叶散抗支气管哮喘作用及机制研究 Δ[J].中国药房,2026,37(05):595-601.
JIN Jiacheng,CHEN Wenyan,LI Xin,et al.Study on the effect and mechanism of Qiwei dongqingye powder against bronchial asthma based on transcriptomics[J].ZHONGGUO YAOFANG,2026,37(05):595-601.
金家成,陈雯艳,李欣,等.基于转录组学的七味冬青叶散抗支气管哮喘作用及机制研究 Δ[J].中国药房,2026,37(05):595-601. DOI: 10.6039/j.issn.1001-0408.2026.05.08.
JIN Jiacheng,CHEN Wenyan,LI Xin,et al.Study on the effect and mechanism of Qiwei dongqingye powder against bronchial asthma based on transcriptomics[J].ZHONGGUO YAOFANG,2026,37(05):595-601. DOI: 10.6039/j.issn.1001-0408.2026.05.08.
目的
2
探讨七味冬青叶散(QDP)抗支气管哮喘的作用及机制。
方法
2
将小鼠分为空白组(生理盐水)、模型组(生理盐水)、地塞米松组(2 mg/kg)和QDP低、中、高剂量组(200、400、800 mg/kg),每组14只。除空白组外,其余各组小鼠腹腔注射+雾化吸入卵清蛋白以复制支气管哮喘模型;造模同时,各组小鼠灌胃/腹腔注射相应药液/生理盐水。末次给药后,观察小鼠肺泡灌洗液(BALF)中的细胞并计数;观察小鼠气管和肺组织的病理学形态;检测小鼠肺组织中丙二醛(MDA)、一氧化氮(NO)、总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)水平,检测小鼠BALF和血清中白细胞介素17(IL-17)水平;采用转录组学预测QDP抗支气管哮喘的作用机制并进行验证。
结果
2
与模型组比较,QDP高剂量组BALF中总细胞数、中性粒细胞数、淋巴细胞数和巨噬细胞数均显著减少(
P
<0.05);肺组织中MDA、NO水平以及BALF和血清中IL-17水平均显著降低(
P
<0.05);肺组织中T-SOD、GSH-Px水平均显著升高(
P
<0.05);肺组织细胞排列趋于正常,炎症细胞浸润减轻,支气管单层柱状上皮细胞脱落减少。转录组学结果显示,差异基因涉及B细胞受体信号传导通路、核因子κB(NF-κB)信号通路、铁死亡信号通路等。进一步验证发现,与模型组比较,QDP各剂量组小鼠肺组织中NF-κB p65、趋化因子配体20表达水平和NF-κB抑制蛋白α磷酸化水平均显著降低(
P
<0.05),核因子E
2
相关因子2(Nrf2)、血红素加氧酶1(HO-1)蛋白表达水平均显著升高(
P
<0.05)。
结论
2
QDP可通过抑制NF-κB信号通路、激活Nrf2/HO-1信号通路,调控氧化应激,减轻炎症反应,从而有效缓解支气管哮喘。
OBJECTIVE
2
To investigate the therapeutic effect and mechanism of Qiwei dongqingye powder (QDP) on bronchial asthma in mice.
METHODS
2
The mice were divided into blank group (normal saline), model group (normal saline), dexamethasone group (2 mg/kg), and QDP low-, medium-, and high-dose groups (200, 400, 800 mg/kg), with 14 mice in each group. Except for the blank group, mice in all other groups were given ovalbumin via intraperitoneal injection followed by aerosol inhalation to induce a bronchial asthma model. During the modeling process, mice in each group were administered corresponding drug solutions or normal saline intragastrically/intraperitoneally. After the last medication, the number of cells in the bronchoalveolar lavage fluid (BALF) of the mice was observed and counted; the pathological changes of the bronchus and lung tissue were observed; the levels of malondialdehyde (MDA), nitric oxide (NO), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px) in the lung tissue of the mice were determined, and the level of interleukin-17 (IL-17) in the BALF and serum was determined. Transcriptomics was employed to predict and validate the mechanism of action of QDP against bronchial asthma.
RESULTS
2
Compared with the model group, the total cell count, neutrophil count, lymphocyte count, and macrophage counts in the BALF of the QDP high-dose group were all significantly reduced (
P
<0.05); the levels of MDA and NO in the lung tissue, and the levels of IL-17 in the BALF and serum were all decreased significantly (
P
<0.05); the levels of T-SOD and GSH-Px were significantly increased (
P
<0.05); the arrangement of lung tissue cells tended to normalize, with reduced infiltration of inflammatory cells and decreased exfoliation of bronchial simple columnar epithelial cells. The transcriptomic results revealed that the differentially expressed genes were B-cell receptor signaling pathway, nuclear factor κB (NF-κB) signaling pathway, ferroptosis signaling pathway, and others. Further validation revealed that, compared with the model group, the expression levels of NF-κB p65 and chemokine ligand 20, as well as the phosphorylation level of NF-κB inhibitor protein α, were significantly decreased in the lung tissues of the mice in all QDP groups (
P
<0.05). Conversely, the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were significantly increased (
P
<0.05).
CONCLUSIONS
2
QDP can effectively alleviate bronchial asthma by inhibiting the NF-κB signaling pathway, activating the Nrf2/HO-1 signaling pathway, regulating oxidative stress, and reducing inflammatory responses.
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