基于miRNA测序分析清肺排毒汤防治小鼠急性肺损伤的分子机制研究

doi:10.12300/j.issn.1674-5817.2025.203

实验动物与比较医学 ›› 2026, Vol. 46 ›› Issue (3): 311-320.DOI: 10.12300/j.issn.1674-5817.2025.203

• 人类疾病动物模型 • 下一篇

基于miRNA测序分析清肺排毒汤防治小鼠急性肺损伤的分子机制研究

李龙雪¹(), 万崇凡², 张琦², 雷茹婷², 王潇玥³, 程乐妍², 赖琦², 刘荣华⁴()(), 刘漩¹()(), 徐铁龙⁵()()

^1.江西中医药大学实验动物科技中心, 南昌 330004
^2.江西中医药大学药学院, 南昌 330004
^3.青岛市中医医院(青岛大学附属青岛市海慈医院), 青岛 266033
^4.江西中医药大学中药药效物质基础江西省重点实验室, 南昌 330004
^5.江西中医药大学循证医学研究中心, 南昌 330004

收稿日期:2025-12-10 修回日期:2026-04-12 出版日期:2026-06-25 发布日期:2026-06-19
通讯作者:
刘荣华（1964—），男，博士，教授，博士生导师，研究方向：中药药效物质基础研究。E-mail： rhliujxucm@163.com。ORCID：0009-0000-7015-6324

刘漩（1989—），女，硕士，讲师，研究方向：中药药效学研究。E-mail： liuxuanglg@126.com。ORCID：0009-0007-9226-5514

徐铁龙（1986—），男，博士，副教授，博士生导师，研究方向：中药抗病毒研究。E-mail： jxciq_xtl@126.com。ORCID：0000-0001-9432-9584
作者简介:李龙雪（1988—），女，硕士，实验师，研究方向：中药药效学研究。E-mail： llx669822@163.com。ORCID：0000-0002-9602-6269
基金资助:
江西省教育厅科学技术研究项目“清肺排毒汤差异调控miRNA-mRNA治疗冠状病毒性肺炎分子机制研究”(GJJ2200921);国家自然科学基金资助项目“清肺排毒汤差异调控miRNA靶向抑制冠状病毒复制研究”(82141214);江西省中医药管理局科技计划项目“清肺排毒汤功能性miRNA表达谱检测及其作用谱研究”(2023A0391);2024年江西省科技专项资金（科技计划第三批）项目“源于经典名方的抗肺结节等现代疾病的中药新药成药性研究”(20243BCC31009);江西省重点实验室组建项目-江西中医药大学“中药药效物质基础江西省重点实验室”(2024SSY07102)

Molecular Mechanisms of Qingfei Paidu Decoction in the Prevention and Treatment of Acute Lung Injury in Mice Based on miRNA Sequencing

LI Longxue¹(), WAN Chongfan², ZHANG Qi², LEI Ruting², WANG Xiaoyue³, CHENG Leyan², LAI Qi², LIU Ronghua⁴()(), LIU Xuan¹()(), XU Tielong⁵()()

^1.Laboratory Animal Science and Technology Center, Jiangxi University of Chinese Medicine, Nanchang 330004, China
^2.School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang 330004, China
^3.Qingdao Traditional Chinese Medicine Hospital, Qingdao Hiser Hospital Affiliated to Qingdao University, Qingdao 266033, China
^4.Jiangxi Provincial Key Laboratory of Effective Material Basis of TCM, Jiangxi University of Chinese Medicine, Nanchang 330004, China
^5.Evidence-Based Medicine Research Center, Jiangxi University of Chinese Medicine, Nanchang 330004, China

Received:2025-12-10 Revised:2026-04-12 Published:2026-06-25 Online:2026-06-19
Contact: LIU Ronghua (ORCID: 0009-0000-7015-6324), E-mail: rhliujxucm@163.com
LIU Xuan (ORCID: 0009-0007-9226-5514), E-mail: liuxuanglg@126.com
XU Tielong(ORCID: 0000-0001-9432-9584), E-mail: jxciq_xtl@126.com

摘要/Abstract

摘要：

目的基于miRNA测序技术探讨清肺排毒汤（Qingfei Paidu decoction，QFPDD）对小鼠急性肺损伤的防治作用及其分子机制。方法 24只4周龄雄性KM小鼠随机分为对照组、模型组和QFPDD组，每组8只。适应性饲养1周后，对照组和模型组灌胃给予超纯水（0.2 mL/次），QFPDD组灌胃给予QFPDD汤剂（0.2 mL/次，含生药1.6 g/mL），2次/d，连续8 d；第2~8天，模型组和QFPDD组给予2.5 g/L脂多糖（lipopolysaccharide，LPS）水溶液4 mL雾化，连续雾化7 d。第9天深度麻醉后通过眼底静脉丛采血，取小鼠肺组织，称取各组小鼠体重和肺组织质量，计算肺系数。采用ELISA法检测小鼠血清中炎症因子肿瘤坏死因子α（tumor necrosis factor-α，TNF-α）、白细胞介素（interleukin，IL）-1β和IL-6水平。对肺组织进行石蜡切片后行HE染色，观察肺组织形态学变化。用Illumina HiSeq 2500测序平台检测小鼠肺组织miRNA表达谱，通过数据库预测差异表达miRNA的靶基因，利用基因本体（gene ontology，GO）和京都基因与基因组数据库（Kyoto Encyclopedia of Genes and Genomes，KEGG）富集分析差异表达miRNA的靶基因功能；通过反转录实时荧光定量PCR技术对差异表达的miRNA进行验证。结果与对照组相比，模型组小鼠体重增长趋势一致，但肺系数显著升高（P＜0.01）。ELISA结果显示，与对照组相比，模型组小鼠血清TNF-α和IL-6水平显著升高（P＜0.01）；与模型组相比，QFPDD组小鼠血清TNF-α和IL-6水平显著降低（P＜0.05）。HE染色结果显示，与对照组相比，模型组小鼠肺泡间隔增宽，大量炎症细胞浸润，部分肺泡扩张，少量毛细血管扩张伴淤血；与模型组相比，QFPDD组小鼠肺泡间隔稍增宽，少量炎症细胞浸润。miRNA测序结合交集分析筛选出模型组与对照组、QFPDD组与模型组之间均存在显著差异的13个miRNA，其中6个miRNA（分别为mmu-miR-203-3p、mmu-miR-181b-5p_R-1、hsa-miR-4286_R+1、mmu-miR-1843b-5p_L+1R-1_2、mmu-miR-22-3p和mmu-miR-1964-3p）在模型组中显著上调（P＜0.05），QFPDD治疗后显著下调（P＜0.05），呈治疗性回调趋势。GO分析显示，差异表达miRNA的靶基因主要富集于RNA聚合酶Ⅱ转录调控等生物学过程。KEGG分析显示，靶基因主要富集于丝裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）信号通路。针对mmu-miR-203-3p的PCR验证结果显示与测序分析结果一致。结论 QFPDD可能通过调控mmu-miR-203-3p等表达，调节炎症反应和MAPK信号通路，参与肺损伤的病理过程，发挥防治急性肺损伤的作用。

关键词: 清肺排毒汤, 急性肺损伤, miR-203-3p, 炎症, MAPK信号通路, KM小鼠

Abstract:

Objective To investigate the preventive and therapeutic effects of Qingfei Paidu decoction (QFPDD) on acute lung injury (ALI) in mice and its underlying molecular mechanisms based on miRNA sequencing technology. Methods Twenty-four 4-week-old male KM mice were randomly divided into a control group, a model group, and a QFPDD group (n = 8 per group). After one week of acclimatization, mice in the control and model groups were intragastrically administered ultrapure water (0.2 mL per dose), whereas mice in the QFPDD group were intragastrically administered QFPDD (1.6 g crude drug/mL, 0.2 mL per dose), twice daily for 8 consecutive days. On days 2–8, mice in the model and QFPDD groups were exposed to aerosolized lipopolysaccharide (LPS) solution (2.5 g/L, 4 mL per exposure) for 7 consecutive days. On day 9, blood was collected via the retro-orbital venous plexus under deep anesthesia, and lung tissues were harvested. Body weight and lung weight were measured, and the lung coefficient was calculated. Serum levels of inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were detected by ELISA. Lung histopathological changes were observed by HE staining of paraffin-embedded sections. miRNA expression profiles in lung tissues were analyzed using the Illumina HiSeq 2500 sequencing platform. Target genes of differentially expressed miRNAs were predicted using bioinformatics databases, and functional enrichment analysis of these target genes was performed using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Differentially expressed miRNAs were validated by reverse transcription quantitative real-time PCR (RT-qPCR). Results Compared with the control group, the model group showed a consistent body weight growth trend but a significantly increased lung coefficient (P < 0.01). ELISA results showed that serum levels of TNF-α and IL-6 were significantly elevated in the model group compared with the control group (P < 0.01), whereas QFPDD treatment significantly reduced serum TNF-α and IL-6 levels compared with the model group (P < 0.05). HE staining showed that, compared with the control group, the model group exhibited widened alveolar septa, massive inflammatory cell infiltration, partial alveolar expansion, and mild capillary dilation with congestion. In contrast, the QFPDD group showed only slightly widened alveolar septa and mild inflammatory cell infiltration compared with the model group. Intersection analysis of miRNA sequencing data identified 13 differentially expressed miRNAs common to both the model vs. control and QFPDD vs. model comparisons. Among them, 6 miRNAs (mmu-miR-203-3p, mmu-miR-181b-5p_R-1, hsa-miR-4286_R+1, mmu-miR-1843b-5p_L+1R-1_2, mmu-miR-22-3p, and mmu-miR-1964-3p) were significantly up-regulated in the model group (P < 0.05) and significantly down-regulated after QFPDD treatment (P < 0.05), showing a therapeutic reversal trend. GO analysis revealed that the target genes of the differentially expressed miRNAs were mainly enriched in biological processes such as RNA polymerase Ⅱ transcriptional regulation. KEGG analysis indicated that target genes were mainly enriched in signaling pathways including the mitogen-activated protein kinase (MAPK) pathway. RT-qPCR validation result for mmu-miR-203-3p was consistent with the sequencing analysis results. Conclusion QFPDD may exert preventive and therapeutic effects against ALI by regulating the expression of mmu-miR-203-3p and other miRNAs, thereby modulating inflammatory responses and the MAPK signaling pathway and participating in the pathological process of lung injury.

Key words: Qingfei Paidu decoction, Acute lung injury, miR-203-3p, Inflammation, MAPK signaling pathway, KM mice

中图分类号:

Q95-33
R-332

李龙雪,李龙雪,万崇凡,等. 基于miRNA测序分析清肺排毒汤防治小鼠急性肺损伤的分子机制研究[J]. 实验动物与比较医学, 2026, 46(3): 311-320. DOI: 10.12300/j.issn.1674-5817.2025.203.

LI Longxue,LI Longxue,WAN Chongfan,et al. Molecular Mechanisms of Qingfei Paidu Decoction in the Prevention and Treatment of Acute Lung Injury in Mice Based on miRNA Sequencing[J]. Laboratory Animal and Comparative Medicine, 2026, 46(3): 311-320. DOI: 10.12300/j.issn.1674-5817.2025.203.

图/表 12

表1 各组小鼠的体重、肺系数和血清炎症因子水平比较 (n=8, x?±s)

Table 1 Comparisons of body weight, lung coefficient, and serum inflammatory factors in different groups of mice

组别

Group

初始体重/g

Initial body weight/g

终末体重/g

Final body weight/g

肺系数/%

Lung coefficient/%

TNF-α

ρ/(pg·mL^-¹)

IL-1β

ρ/(pg·mL^-¹)

IL-6

ρ/(pg·mL^-¹)

对照组

Control group

模型组

Model group

QFPDD 组

QFPDD group

表1 各组小鼠的体重、肺系数和血清炎症因子水平比较 (n=8, x?±s)

Table 1 Comparisons of body weight, lung coefficient, and serum inflammatory factors in different groups of mice

组别

Group

初始体重/g

Initial body weight/g

终末体重/g

Final body weight/g

肺系数/%

Lung coefficient/%

TNF-α

ρ/(pg·mL^-¹)

IL-1β

ρ/(pg·mL^-¹)

IL-6

ρ/(pg·mL^-¹)

对照组

Control group

模型组

Model group

QFPDD 组

QFPDD group

注：对照组，连续8 d灌胃给予超纯水；模型组，第1天灌胃给予超纯水，第2～8天给予脂多糖（LPS）水溶液雾化，建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化以建立模型。×200标尺为100 μm，×400标尺为50 μm；红色箭头指示炎症细胞浸润，红色五角星指示毛细血管扩张淤血。
">

图1 各组小鼠肺组织HE染色结果
注：对照组，连续8 d灌胃给予超纯水；模型组，第1天灌胃给予超纯水，第2～8天给予脂多糖（LPS）水溶液雾化，建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化以建立模型。×200标尺为100 μm，×400标尺为50 μm；红色箭头指示炎症细胞浸润，红色五角星指示毛细血管扩张淤血。

Figure 1 HE staining of lung tissues from mice in different groups
Note： Control group， intragastrically administered ultrapure water for 8 consecutive days. Model group， intragastrically administered ultrapure water on day 1， followed by exposure to aerosolized lipopolysaccharide （LPS） solution on days 2–8 to establish the acute lung injury （ALI） model. QFPDD group， intragastrically administered Qingfei Paidu decoction （QFPDD） for 8 consecutive days， with concurrent exposure to aerosolized LPS solution on days 2–8 for ALI induction. Scale bars： 100 μm （×200） and 50 μm （×400）. Red arrows indicate inflammatory cell infiltration； red stars indicate capillary dilation and congestion.

注：A，韦恩图，橙色圆圈代表QFPDD组与模型组相比具有显著性变化的miRNA个数，蓝色圆圈代表模型组与对照组相比具有显著性变化的miRNA个数，重叠部分代表两次比较中共有的miRNA个数。B，与QFPDD的潜在防治效应相关的miRNA表达量变化。对照组，连续8 d灌胃给予超纯水；模型组，灌胃给予超纯水1 d，然后于第2～8天给予脂多糖（LPS）水溶液雾化以建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化建模。每组随机选取4只小鼠的肺组织，与对照组比较，^*P＜0.05，^**P＜0.01；与模型组比较，^#P＜0.05，^##P＜0.01。
">

图2 miRNA测序分析各组小鼠肺组织中差异表达的miRNA
注：A，韦恩图，橙色圆圈代表QFPDD组与模型组相比具有显著性变化的miRNA个数，蓝色圆圈代表模型组与对照组相比具有显著性变化的miRNA个数，重叠部分代表两次比较中共有的miRNA个数。B，与QFPDD的潜在防治效应相关的miRNA表达量变化。对照组，连续8 d灌胃给予超纯水；模型组，灌胃给予超纯水1 d，然后于第2～8天给予脂多糖（LPS）水溶液雾化以建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化建模。每组随机选取4只小鼠的肺组织，与对照组比较，^*P＜0.05，^**P＜0.01；与模型组比较，^#P＜0.05，^##P＜0.01。

Figure 2 Differentially expressed miRNAs in lung tissues of mice among groups detected by miRNA sequencing
Note： A， Venn diagram. The orange circle represents the number of miRNAs with significant changes in the QFPDD group compared with the model group. The blue circle represents the number of miRNAs with significant changes in the model group compared with the control group. The overlapping section represents the number of miRNAs shared in both comparisons. B， Changes in the expression levels of miRNAs associated with the potential preventive and therapeutic effects of QFPDD. Control group， intragastrically administered ultrapure water for 8 consecutive days. Model group， intragastrically administered ultrapure water on day 1， followed by exposure to aerosolized lipopolysaccharide （LPS） solution on days 2–8 to establish the acute lung injury （ALI） model. QFPDD group， intragastrically administered Qingfei Paidu decoction （QFPDD） for 8 consecutive days， with concurrent exposure to aerosolized LPS solution on days 2–8 for ALI induction. Lung tissues from 4 randomly selected mice per group were used （n=4）. Compared with the control group， ^*P < 0.05， ^**P < 0.01； compared with the model group， ^#P < 0.05， ^##P < 0.01.

图3 差异表达miRNA的靶基因GO富集分析

Figure 3 GO enrichment analysis of target genes of differentially expressed miRNAs

图3 差异表达miRNA的靶基因GO富集分析

Figure 3 GO enrichment analysis of target genes of differentially expressed miRNAs

注：A，QFPDD组和模型组相比，具有显著变化的miRNA靶基因的KEGG富集分析；B，靶向丝裂原活化蛋白激酶（MAPK）信号通路的前20位miRNA表达热图。C2、C6、C9和C26为对照组；M8、M10、M64和M68为模型组；Q3、Q7、Q11和Q12为清肺排毒汤组。
">

图 4 差异表达 miRNA的靶基因KEGG富集分析
注：A，QFPDD组和模型组相比，具有显著变化的miRNA靶基因的KEGG富集分析；B，靶向丝裂原活化蛋白激酶（MAPK）信号通路的前20位miRNA表达热图。C2、C6、C9和C26为对照组；M8、M10、M64和M68为模型组；Q3、Q7、Q11和Q12为清肺排毒汤组。

Figure 4 KEGG enrichment analysis of target genes for differentially expressed miRNAs
Note： A， KEGG enrichment analysis of target genes for miRNAs with significant changes in the QFPDD group compared to the model group； B， Heatmap of expression levels of the top 20 miRNAs targeting the mitogen-activated protein kinase （MAPK） signaling pathway. C2， C6， C9， and C26 are the control group； M8， M10， M64， and M68 are the model group； Q3， Q7， Q11，and Q12 are QFPDD group.

注：对照组，连续8 d灌胃给予超纯水；模型组，灌胃给予超纯水1 d，然后于第2～8天给予脂多糖（LPS）水溶液雾化建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化建模。每组随机选取4只小鼠的肺组织进行实时荧光定量PCR分析。与对照组相比，^**P＜0.01；与模型组相比，^##P＜0.01。
">

图 5 实时荧光定量PCR验证mmu-miR-203-3p差异表达
注：对照组，连续8 d灌胃给予超纯水；模型组，灌胃给予超纯水1 d，然后于第2～8天给予脂多糖（LPS）水溶液雾化建立急性肺损伤模型；QFPDD组，连续8 d灌胃给予清肺排毒汤（QFPDD），并于第2～8天给予LPS水溶液雾化建模。每组随机选取4只小鼠的肺组织进行实时荧光定量PCR分析。与对照组相比，^**P＜0.01；与模型组相比，^##P＜0.01。

Figure 5 Validation of differential expression of mmu-miR-203-3p by quantitative real-time PCR
Note： Control group， intragastrically administered ultrapure water for 8 consecutive days. Model group， intragastrically administered ultrapure water on day 1， followed by exposure to aerosolized lipopolysaccharide （LPS） solution on days 2–8 to establish the acute lung injury （ALI） model. QFPDD group， intragastrically administered Qingfei Paidu decoction （QFPDD） for 8 consecutive days， with concurrent exposure to aerosolized LPS solution on days 2–8 for ALI induction. Lung tissues from 4 randomly selected mice per group were used for quantitative real-time PCR analysis （n=4）. Compared with the control group， ^**P < 0.01； compared with the model group， ^##P < 0.01.

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基于miRNA测序分析清肺排毒汤防治小鼠急性肺损伤的分子机制研究

Molecular Mechanisms of Qingfei Paidu Decoction in the Prevention and Treatment of Acute Lung Injury in Mice Based on miRNA Sequencing

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