旱莲苷A通过调控JAK2/STAT3通路抑制M1型巨噬细胞极化改善葡聚糖硫酸钠诱导的小鼠结肠炎

doi:10.12122/j.issn.1673-4254.2025.06.19

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (6): 1297-1306.doi: 10.12122/j.issn.1673-4254.2025.06.19

旱莲苷A通过调控JAK2/STAT3通路抑制M1型巨噬细胞极化改善葡聚糖硫酸钠诱导的小鼠结肠炎

牛民主¹^,⁴^,⁵(), 殷丽霞², 乔通⁴, 尹林², 张可妮², 胡建国¹^,², 宋传旺⁴, 耿志军¹^,³, 李静¹^,²()

^1.蚌埠医科大学第一附属医院，炎症相关性疾病基础与转化研究安徽省重点实验室，安徽蚌埠 233004
^2.蚌埠医科大学第一附属医院，检验科，安徽蚌埠 233004
^3.蚌埠医科大学第一附属医院，中心实验室，安徽蚌埠 233004
^4.蚌埠医科大学检验医学院免疫学教研室，安徽蚌埠 233030
^5.安徽医科大学附属宿州医院输血科，安徽宿州 234000

收稿日期:2025-01-20 出版日期:2025-06-20 发布日期:2025-06-27
通讯作者: 李静 E-mail:nmz8033@163.com;lijingbyfy@bbmc.edu.cn
作者简介:牛民主，在读硕士研究生，E-mail: nmz8033@163.com
基金资助:
安徽高校自然科学研究项目优秀青年项目(2022AH030138);安徽省临床医学研究转化项目(202427b10020088);蚌埠医科大学第一附属医院基金项目创新团队项目(BYYFY2022TD002)

Ecliptasaponin A ameliorates DSS-induced colitis in mice by suppressing M1 macrophage polarization via inhibiting the JAK2/STAT3 pathway

Minzhu NIU¹^,⁴^,⁵(), Lixia YIN², Tong QIAO⁴, Lin YIN², Keni ZHANG², Jianguo HU¹^,², Chuanwang SONG⁴, Zhijun GENG¹^,³, Jing LI¹^,²()

^1.Anhui Provincial Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China
^2.Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China
^3.Central Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China
^4.Department of Immunology, School of Laboratory Medicine, Bengbu Medical University, Bengbu 233030, China
^5.Department of Blood Transfusion, Suzhou Hospital of Anhui Medical University, Suzhou 234000, China

Received:2025-01-20 Online:2025-06-20 Published:2025-06-27
Contact: Jing LI E-mail:nmz8033@163.com;lijingbyfy@bbmc.edu.cn

摘要/Abstract

摘要：

目的探讨旱莲苷A（ESA）对葡聚糖硫酸钠（DSS）诱导的小鼠炎症性肠病（IBD）模型的影响及其对巨噬细胞极化的作用机制。方法体内实验采用24只8~10周龄雄性C57BL/6小鼠，随机分成对照组（WT组）、2.5% DSS诱导模型组（DSS组）、ESA治疗组（DSS+ESA组，50 mg/kg），8只/组。每日记录小鼠体质量，观察粪便性状，通过DAI评分、结肠长度、脾指数、结肠组织HE染色及组织炎症评分、ELISA和RT-qPCR检测的肠黏膜炎症介质（TNF-α、IL-6和iNOS）水平评估ESA对小鼠肠炎症状的影响；采用AB-PAS染色标记杯状细胞，免疫荧光和Western blotting检测紧密连接蛋白水平（ZO-1和Claudin-1），评估ESA对小鼠肠道屏障的作用。体外培养小鼠单核巨噬细胞白血病细胞RAW264.7，分为Control组（M0组）、LPS（1 μg/mL）+IFN-γ（20 ng/mL）诱导组（M1组）和ESA治疗组（ESA组，50 μmol/L），采用流式细胞术评估ESA对小鼠肠系膜淋巴结及体外模型M1型极化标志物（CD86）比例的影响。Western blotting检测JAK2/STAT3通路关键蛋白表达，并使用信号通路激活剂RO8191（20 μmol/L）干预，分析ESA调控巨噬细胞极化的分子机制。结果体内实验显示，ESA可明显缓解DSS诱导的小鼠体质量下降、结肠长度缩短及DAI评分、脾指数、组织炎症评分的升高（P<0.05）；HE结果显示，ESA可保护肠道固有层，减轻肠道炎症细胞浸润；ELISA和RT-qPCR显示，ESA可抑制DSS诱导的小鼠肠黏膜组织相关炎症介质（TNF-α、IL-6和iNOS）的高表达（P<0.05）；AB-PAS和免疫荧光结果显示，ESA可保护结肠组织杯状细胞、黏液屏障和机械屏障的损伤。流式细胞术结果发现，ESA可降低DSS诱导的小鼠肠系膜淋巴结和体外诱导的M1型巨噬细胞极化标志物（CD86）的阳性比例（P<0.05）。Western blotting结果显示，体内外ESA治疗组p-JAK2和p-STAT3水平低于诱导组（P<0.05）；体外经JAK2/STAT3激活剂RO8191干预后显示，ESA药物治疗未能抑制JAK2/STAT3信号通路活化，同时M1型极化标志物CD86阳性比例增加（P<0.05）。结论 ESA可靶向拮抗JAK2/STAT3通路活化介导的M1型巨噬细胞极化，抑制炎症因子导致的肠道屏障的损伤，从而缓解DSS诱导的小鼠结肠炎。

关键词: 旱莲苷A, 炎症性肠病, 肠屏障, 巨噬细胞极化, JAK2/STAT3

Abstract:

Objective To investigate the effect of ecliptasaponin A (ESA) for alleviating dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD) in mice and the underlying mechanism. Methods Twenty-four male C57BL/6 mice (8-10 weeks old) were equally randomized into control group, DSS-induced IBD model group, and DSS+ESA (50 mg/kg) treatment group. Disease activity index (DAI), colon length and spleen index of the mice were measured, and intestinal pathology was examined with HE staining. The expressions of inflammatory mediators (TNF-α, IL-6, and iNOS) in the colon mucosa were detected using ELISA and RT-qPCR, and intestinal barrier integrity was assessed using AB-PAS staining and by detecting ZO-1 and claudin-1 expressions using immunofluorescence staining and Western blotting. In cultured RAW264.7 macrophages, the effects of treatment with 50 μmol/L ESA, alone or in combination with 20 μmol/L RO8191 (a JAK2/STAT3 pathway activator), on M1 polarization of the cells induced by LPS and IFN-γ stimulation and expressions of JAK2/STAT3 pathway proteins were analyzed using flow cytometry and Western blotting. Results In the mouse models of DSS-induced IBD, ESA treatment significantly alleviated body weight loss and colon shortening, reduced DAI, spleen index and histological scores, and ameliorated inflammatory cell infiltration in the colon tissue. ESA treatment also suppressed TNF‑α, IL-6 and iNOS expressions, protected the goblet cells and the integrity of the mucus and mechanical barriers, and upregulated the expressions of ZO-1 and claudin-1. ESA treatment obviously decreased CD86⁺ M1 polarization in the mesenteric lymph nodes of IBD mice and in LPS and IFN-γ-induced RAW264.7 cells, and significantly reduced p-JAK2 and p-STAT3 expressions in both the mouse models and RAW264.7 cells. Treatment with RO8191 caused reactivation of JAK2/STAT3 and strongly attenuated the inhibitory effect of ESA on CD86⁺ polarization in RAW264.7 cells. Conclusion ESA alleviates DSS-induced colitis in mice by suppressing JAK2/STAT3-mediated M1 macrophage polarization and mitigating inflammation-driven intestinal barrier damage.

Key words: ecliptasaponin A, inflammatory bowel disease, intestinal barrier, macrophage polarization, JAK2/STAT3

牛民主, 殷丽霞, 乔通, 尹林, 张可妮, 胡建国, 宋传旺, 耿志军, 李静. 旱莲苷A通过调控JAK2/STAT3通路抑制M1型巨噬细胞极化改善葡聚糖硫酸钠诱导的小鼠结肠炎[J]. 南方医科大学学报, 2025, 45(6): 1297-1306.

Minzhu NIU, Lixia YIN, Tong QIAO, Lin YIN, Keni ZHANG, Jianguo HU, Chuanwang SONG, Zhijun GENG, Jing LI. Ecliptasaponin A ameliorates DSS-induced colitis in mice by suppressing M1 macrophage polarization via inhibiting the JAK2/STAT3 pathway[J]. Journal of Southern Medical University, 2025, 45(6): 1297-1306.

图/表 8

图1 ESA显著降低体外模型M1型巨噬细胞的比例

Fig.1 ESA significantly reduces percentage of M1-type macrophages in RAW264.7 cells induced by LPS and IFN-γ. A: Morphology of macrophages from each group (scale bar=50 μm). B: Percentages of F4/80+CD86+ macrophages detected by flow cytometry. *P<0.05 vs M0 group. #P<0.05 vs M1 group.

图2 ESA对DSS模型小鼠疾病状态的影响

Fig.2 Effect of ESA on the disease status of DSS model mice. A: Changes of body weight. B: Changes of DAI scores. WT: Control group; DSS: DSS-induced model group; DSS+ESA: ESA treatment group. *P<0.05 vs WT group. #P<0.05 vs DSS group.

图3 ESA改善DSS诱导的结肠炎的病理表型

Fig.3 ESA improves pathological phenotype of DSS-induced colitis in mice. A, B: Representative images of mouse colons in each group. C: Changes of spleen index. D: HE staining of the colon tissues. E: AB-PAS staining of colon tissue from each groups. F: Histopathological scores in different groups. *P<0.05 vs WT group. #P<0.05 vs DSS group. (scale bar=100 μm).

图4 ESA对DSS模型小鼠肠黏膜炎症介质的影响

Fig.4 Effect of ESA on intestinal mucosal inflammatory mediators in DSS model mice. A-C: Concentrations of proinflammatory cytokines TNF-α, iNOS and IL-6 in the colon tissues detected by ELISA. D-F: The mRNA levels of proinflammatory cytokines TNF-α, iNOS and IL-6 in different groups. *P<0.05 vs WT group. #P<0.05 vs DSS group.

图5 ESA减轻DSS诱导的结肠炎的肠道屏障破坏

Fig.5 ESA improves gut barrier disruption in mice with DSS-induced colitis. A: Immunofluorescence staining showing expression of ZO-1 and claudin-1 proteins in the colon tissues. B, C: Relative expression levels of ZO-1 and claudin-1 proteins in colon mucosa detected by Western blotting. *P<0.05 vs WT group. #P<0.05 vs DSS group (scale bar=100 μm).

图6 ESA对DSS模型小鼠肠系膜淋巴结中M1型巨噬细胞的影响

Fig.6 Effect of ESA on M1 macrophages in the mesenteric lymph nodes of DSS model mice. The percentages of F4/80+CD86+ macrophages in mesenteric lymph nodes were detected by flow cytometry. *P<0.05 vs WT group. #P<0.05 vs DSS group.

图7 ESA可抑制体内外JAK2/STAT3信号通路的磷酸化

Fig.7 ESA suppresses JAK2/STAT3 pathway activation by blocking its phosphorylation in vitro and in vivo. A, B: Relative expression levels of JAK2, p-JAK2, STAT3, and p-STAT3 proteins in mouse colon tissue detected by Western blotting (*P<0.05 vs WT group; #P<0.05 vs DSS group). C, D: Relative expression levels of JAK2, p-JAK2, STAT3, p-STAT3 proteins in RAW264.7 cells detected by Western blotting (*P<0.05 vs M0 group. #P<0.05 vs M1 group).

图8 JAK2/STAT3信号通路参与ESA抑制M1型巨噬细胞极化

Fig.8 JAK2/STAT3 signaling pathway is involved in ESA-mediated inhibition of M1-type macrophage polarization of RAW264.7 cells. A, B: Relative expressions of JAK2, p-JAK2, STAT3 and p-STAT3 proteins detected by Western blotting in RAW264.7 cells. C: Morphology of the macrophages (×400). D: Proportion of F4/80+CD86+ cells in each group. *P<0.05 vs ESA group (Scale bar=50 μm).

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旱莲苷A通过调控JAK2/STAT3通路抑制M1型巨噬细胞极化改善葡聚糖硫酸钠诱导的小鼠结肠炎

Ecliptasaponin A ameliorates DSS-induced colitis in mice by suppressing M1 macrophage polarization via inhibiting the JAK2/STAT3 pathway

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