艾黄素对臭氧暴露诱发小鼠肺部炎症的保护作用及机制研究

doi:10.12300/j.issn.1674-5817.2026.003

实验动物与比较医学 ›› 2026, Vol. 46 ›› Issue (5): 640-649.DOI: 10.12300/j.issn.1674-5817.2026.003

• 实验动物与中药学研究 • 上一篇下一篇

艾黄素对臭氧暴露诱发小鼠肺部炎症的保护作用及机制研究

李燕平¹^,²(), 黄姗¹^,², 姚政源¹^,², 石怡敏², 隋华秀¹^,², 黄侯丹², 俞燕萍², 米燕¹^,², 林大晖¹^,²()()

^1. 厦门医学院机能与临床转化福建高校重点实验室, 厦门 361023
^2. 厦门医学院基础医学院, 厦门 361023

收稿日期:2026-01-04 修回日期:2026-06-04 出版日期:2026-10-25 发布日期:2026-10-16
通讯作者: 林大晖（1980—），男，博士，副教授，研究方向：免疫微环境与药物偶联。E-mail：tahui.lin@foxmail.com。ORCID：0000-0001-7627-6095
作者简介:
李燕平（1987—），女，学士，实验师，研究方向：呼吸系统疾病防治。E-mail：201900010478@xmmc.edu.cn。ORCID：0009-0004-7088-3598
基金资助:
福建省中青年教师教育科研项目（科技类）“艾黄素及其衍生物抗炎作用机制研究”(JAT241176)

Protective Effect and Mechanism of Artemitin on Ozone-Induced Pulmonary Inflammation in Mice

LI Yanping¹^,²(), HUANG Shan¹^,², YAO Jengyuan¹^,², SHI Yimin², SUI Huaxiu¹^,², HUANG Houtan², YU Yanping², MI Yan¹^,², LIN Tahui¹^,²()()

^1. Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Xiamen 361023, China
^2. School of Basic Medical Sciences, Xiamen Medical College, Xiamen 361023, China

Received:2026-01-04 Revised:2026-06-04 Published:2026-10-25 Online:2026-10-16
Correspondence to:
LIN Tahui (ORCID: 0000-0001-7627-6095), E-mail: tahui.lin@foxmail.com

摘要/Abstract

摘要：

目的探讨艾黄素（artemitin）对臭氧暴露诱发的小鼠肺部炎症是否具有保护作用及其潜在机制。方法将32只雄性SPF级C57BL/6小鼠随机分为空白对照组、艾黄素对照组、模型组、艾黄素治疗组，每组8只。艾黄素治疗组每日先腹腔注射艾黄素（20 mg/kg），再持续吸入0.000 25%臭氧1 h；艾黄素对照组每日先腹腔注射艾黄素（20 mg/kg），再吸入洁净空气；模型组每日先腹腔注射等体积生理盐水，再吸入0.000 25%臭氧1 h；空白对照组每日先注射等体积生理盐水，再吸入洁净空气；以上各组均连续处理7 d。采用全身体积描记检测系统检测各组小鼠的肺功能指标；采用ELISA检测支气管肺泡灌洗液中肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白细胞介素-1β（interleukin-1β，IL-1β）水平；采用HE染色观察肺组织病理学变化；并采用超高效液相色谱质谱联用对血浆中整体代谢通路的变化进行非靶向代谢组学分析。结果与模型组相比，艾黄素治疗能显著改善臭氧引起的肺功能损伤（P<0.05）、降低支气管肺泡灌洗液中TNF-α、IL-1β的蛋白水平（P<0.05）、减轻肺组织炎症细胞浸润和结构破坏。代谢组学结果提示，艾黄素治疗可代偿性增强能量供给和氧化脂质信号，抑制嘌呤代谢与色氨酸衍生通路。结论艾黄素对臭氧暴露诱发的小鼠肺部炎症具有明显的保护作用，其通过协同调控色氨酸代谢、能量代谢和脂质炎症介质，从代谢层面改善代谢紊乱，进而抑制下游炎症反应与气道高反应性。本研究不仅揭示了艾黄素治疗气道炎症的多效性机制，还为其临床转化提供了潜在的代谢生物标志物和理论依据。

关键词: 臭氧, 艾黄素, 肺部炎症, 肿瘤坏死因子-α, 白细胞介素-1β, C57BL/6小鼠

Abstract:

Objective To investigate the protective effect of artemitin against ozone (O₃)-induced pulmonary inflammation in mice and to explore its underlying mechanism. Methods Thirty-two specific pathogen-free (SPF) male C57BL/6 mice were randomly divided into a blank control group, an artemitin-only control group, an O₃-induced model group, and an artemitin-treated group, with 8 mice in each group. In the artemitin-treated group, animals were injected intraperitoneally with artemitin (20 mg/kg) daily, followed by a 1 h exposure to 0.000 25% O₃. The artemitin-only control group received the same artemitin injection but was exposed to clean air. The O₃-induced model group was injected intraperitoneally with an equal volume of normal saline daily, followed by a 1-h exposure to 0.000 25% O₃. The blank control group received the saline injection and was exposed to clean air. All treatments were administered for 7 consecutive days. Pulmonary function indices of the mice in each group were measured using a whole-body plethysmography system. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (HE) staining was used to observe the histopathological changes in the lung tissue, and ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was employed for untargeted metabolomic analysis to examine the changes in overall metabolic pathways in plasma. Results Compared with the O₃-induced model group, artemitin treatment significantly improved O₃-induced lung function impairments (P<0.05), lowered the levels of TNF-α and IL-1β in BALF (P<0.05) and alleviated inflammatory cell infiltration and structural damage in lung tissues. Metabolomics results indicated that artemitin treatment compensatorily enhanced energy supply and oxidized lipid signaling, while inhibiting purine metabolism and tryptophan-derived pathways. Conclusion Artemitin exhibits a significant protective effect against O₃-induced pulmonary inflammation in mice. It corrects upstream metabolic disorders by synergistically modulating tryptophan metabolism, energy metabolism, and lipid inflammatory mediators, thereby inhibiting downstream inflammatory responses and airway hyperresponsiveness. This study not only reveals the pleiotropic mechanism of artemitin in treating airway inflammation but also provides potential metabolic biomarkers and a theoretical basis for its clinical translation.

Key words: Ozone, Artemitin, Pulmonary inflammation, Tumor necrosis factor-α, Interleukin-1β, C57BL/6 mice

中图分类号:

R-332
R563

李燕平,黄姗,姚政源,等. 艾黄素对臭氧暴露诱发小鼠肺部炎症的保护作用及机制研究[J]. 实验动物与比较医学, 2026, 46(5): 640-649. DOI: 10.12300/j.issn.1674-5817.2026.003.

LI Yanping,HUANG Shan,YAO Jengyuan,et al. Protective Effect and Mechanism of Artemitin on Ozone-Induced Pulmonary Inflammation in Mice[J]. Laboratory Animal and Comparative Medicine, 2026, 46(5): 640-649. DOI: 10.12300/j.issn.1674-5817.2026.003.

图/表 5

图1 实验流程图

注：RR，呼吸频率；TV，潮气量；MV，每分通气量；Penh，增强间歇值；PAU，呼吸暂停；PIF，最大吸气流量；PEF，最大呼气流量；Ti，吸气时间；Te，呼气时间；EF₅₀，呼气中期流速；TNF-α，肿瘤坏死因子α；IL-1β，白细胞介素-1β。

Figure 1 Experimental flowchart

Note： RR， respiratory rate； TV， tidal volume； MV， minute ventilation； Penh， enhanced pause； PAU， pause； PIF， peak inspiratory flow； PEF， peak expiratory flow； Ti， inspiratory time； Te， expiratory time； EF₅₀， expiratory flow at 50% tidal volume； TNF-α， tumor necrosis factor -α； IL-1β， interleukin-1β.

图2 小鼠肺功能的检测结果和支气管肺泡灌洗液中炎症因子TNF-α、IL-1β的水平

注：A～J，空白对照组、艾黄素对照组、模型组、艾黄素治疗组小鼠肺功能各指标（Penh、PAU、Te、MV、EF₅₀、PEF、RR、TV、PIF、Ti）的检测结果；K～L，空白对照组、艾黄素对照组、模型组、艾黄素治疗组小鼠支气管肺泡灌洗液中炎症因子TNF-α和IL-1β的水平。艾黄素治疗组每日先腹腔注射艾黄素（20 mg/kg），再持续吸入体积分数为0.000 25% O₃ 1 h；艾黄素对照组每日先腹腔注射艾黄素（20 mg/kg），再吸入洁净空气；模型组每日先腹腔注射等体积生理盐水，再持续吸入体积分数为0.000 25% O₃ 1 h；空白对照组每日先注射等体积生理盐水，再吸入洁净空气；以上各组均连续处理7 d。Penh，增强间歇值；PAU，呼吸暂停；Te，呼气时间；MV，每分通气量；EF₅₀，呼气中期流速；PEF，最大呼气流量；RR，呼吸频率；TV，潮气量；PIF，最大吸气流量；Ti，吸气时间；TNF-α，肿瘤坏死因子α；IL-1β，白细胞介素-1β。n=8；^ns P>0.05，^** P<0.01，^*** P<0.001，^**** P<0.000 1。

Figure 2 Pulmonary function indicators and levels of inflammatory factors TNF-α and IL-1β in bronchoalveolar lavage fluid of mice

Note： A-J， Detection results of various pulmonary function indices （Penh， PAU， Te， MV， EF₅₀， PEF， RR， TV， PIF， Ti） of mice in the blank control group， artemitin-only control group， model group， and artemitin-treated group； K-L， Levels of inflammatory factors TNF-α and IL-1β in bronchoalveolar lavage fluid of mice in the blank control group， artemitin-only control group， model group， and artemitin-treated group. The artemitin-treated group was first intraperitoneally injected with artemitin （20 mg/kg） each day， and then continuously exposed to 0.000 25% O₃ for 1 h； the artemitin-only control group was first intraperitoneally injected with artemitin （20 mg/kg） each day， and then exposed to clean air； the O₃-induced model group was first intraperitoneally injected with an equal volume of normal saline each day， and then exposed to 0.000 25% O₃ for 1 h； the blank control group was first injected with an equal volume of normal saline each day， and then exposed to clean air； all the above groups were continuously treated for 7 d. Penh， enhanced pause； PAU， pause； Te， expiratory time； MV， minute ventilation； EF₅₀， expiratory flow at 50% tidal volume； PEF， peak expiratory flow； RR， respiratory rate； TV， tidal volume； PIF， peak inspiratory flow； Ti， inspiratory time； TNF-α， tumor necrosis factor-α； IL-1β， interleukin-1β. n=8； ^ns P>0.05， ^** P<0.01， ^*** P<0.001， ^**** P<0.000 1.

图2 小鼠肺功能的检测结果和支气管肺泡灌洗液中炎症因子TNF-α、IL-1β的水平

Figure 2 Pulmonary function indicators and levels of inflammatory factors TNF-α and IL-1β in bronchoalveolar lavage fluid of mice

图3 小鼠肺组织的HE染色结果

注：艾黄素治疗组每日先腹腔注射艾黄素（20 mg/kg），再持续吸入0.000 25% O₃ 1 h；艾黄素对照组每日先腹腔注射艾黄素（20 mg/kg），再吸入洁净空气；模型组每日先腹腔注射等体积生理盐水，再吸入0.000 25% O₃ 1 h；空白对照组每日先注射等体积生理盐水，再吸入洁净空气；以上各组均连续处理7 d。

Figure 3 Results of HE staining of lung tissues in mice

Note： The artemitin-treated group was first intraperitoneally injected with artemitin （20 mg/kg） each day， and then continuously exposed to 0.000 25% O₃ for 1 h； the artemitin-only control group was first intraperitoneally injected with artemitin （20 mg/kg） each day， and then exposed to clean air； the O₃-induced model group was first intraperitoneally injected with an equal volume of normal saline each day， and then exposed to 0.000 25% O₃ for 1 h； the blank control group was first injected with an equal volume of normal saline each day， and then exposed to clean air； all the above groups were continuously treated for 7 d.

图 4 代谢组学多变量统计与KEGG富集分析结果

注：A，空白对照组、模型组和艾黄素治疗组小鼠血浆在ESI⁺模式下的主成分分析（PCA）得分图；B，空白对照组、模型组和艾黄素治疗组小鼠血浆在ESI⁻模式下的PCA得分图；C，模型组与艾黄素治疗组小鼠血浆在ESI⁺模式下的正交偏最小二乘判别分析（OPLS-DA）得分图；D，模型组与艾黄素治疗组小鼠血浆在ESI⁻模式下的OPLS-DA得分图；E，模型组与艾黄素治疗组差异代谢物火山图；F，差异代谢物KEGG通路富集分析排名前10位的通路。ESI，电喷雾离子化；PCA，主成分分析；OPLS-DA，正交偏最小二乘判别分析；FC，倍数变化。n=8。

Figure 4 Multivariate statistical and KEGG enrichment analysis in metabolomics

Note： A， PCA score plots of plasma from the blank control， O₃-induced model， and artemitin-treated groups in ESI⁺ mode； B， PCA score plots of plasma from the blank control， O₃-induced model， and artemitin-treated groups in ESI⁻ mode； C， OPLS-DA score plots of plasma from the O₃-induced model and artemitin-treated groups in ESI⁺ mode； D， OPLS-DA score plots of plasma from the O₃-induced model and artemitin-treated groups in ESI⁻ mode； E， Volcano plot of differential metabolites between the O₃-induced model and artemitin-treated groups； F， Top 10 enriched KEGG pathways of differential metabolites. ESI， electrospray ionization； PCA， principal component analysis； OPLS-DA， orthogonal partial least squares discriminant analysis； FC， fold change. n=8.

表 1

艾黄素治疗组与模型组血浆中的差异代谢物

Table 1

Differential metabolites in plasma between the artemitin-treated group and the O₃-induced model group

序号No.	质荷比 m/z	化合物 Compound	KEGG编号 KEGG ID	HMDB编号 HMDB ID	log₂FC	-log₁₀ P	AUC	保留时间/min Retention time/min	离子化模式 Ionization mode
1	103.040 818 5	3-Hydroxybutyric acid	C01089	HMDB0000011	1.8	10.1	1.00	0.76	negative
2	361.203 087 3	Cortisol	C00735	HMDB0000063	2.4	7.3	1.00	1.08	negative
3	363.218 000 8	Leukotriene A4	C00909	HMDB0001337	3.2	6.8	1.00	1.34	negative
4	160.077 502 2	Phenylacetaldehyde	C00601	HMDB0006236	-2.2	6.0	0.98	0.93	negative
5	307.115 643 5	Adenosine	C00212	HMDB0000050	-2.0	7.8	0.97	0.77	negative
6	160.041 370 6	Quinoline-4,8-diol	C05637	HMDB0060289	-1.2	6.2	0.97	0.90	negative
7	131.048 605 8	N1-Acetyl-N2-formyl-5-methoxykynuramine	C05642	HMDB0004259	-1.6	5.6	0.96	0.94	positive
8	496.274 317 6	Taurocholic acid	C05122	HMDB0000036	1.7	4.6	0.95	3.07	negative
9	311.224 870 9	12,13-EpOME	C14826	HMDB0004702	1.0	5.2	0.95	3.25	negative
10	360.071 196 1	N-Glycolylneuraminic acid	C03410	HMDB0000833	-2.7	5.1	0.93	0.87	negative
11	283.083 160 1	6-Hydroxymelatonin	C05643	HMDB0004081	2.0	4.6	0.95	0.80	negative
12	235.083 009 7	5-Formiminotetrahydrofolic acid	C00664	HMDB0001534	1.8	7.3	0.95	0.77	negative
13	147.012 513 4	Oxoglutaric acid	C00026	HMDB0000208	2.1	3.8	0.89	8.24	positive
14	187.008 039 0	3-Fumarylpyruvate	C02514	HMDB0060371	1.5	4.0	0.86	0.84	negative
15	208.062 677 7	Homogentisic acid	C00544	HMDB0000130	1.5	3.8	0.82	0.77	negative

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艾黄素对臭氧暴露诱发小鼠肺部炎症的保护作用及机制研究

Protective Effect and Mechanism of Artemitin on Ozone-Induced Pulmonary Inflammation in Mice

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