升麻素抑制MAPK通路调节辅助性T细胞免疫平衡改善小鼠克罗恩病样结肠炎

doi:10.12122/j.issn.1673-4254.2025.03.17

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (3): 595-602.doi: 10.12122/j.issn.1673-4254.2025.03.17

• • 上一篇

升麻素抑制MAPK通路调节辅助性T细胞免疫平衡改善小鼠克罗恩病样结肠炎

殷丽霞¹^,³(), 牛民主², 张可妮¹^,³, 耿志军², 胡建国¹^,², 李江艳¹^,², 李静¹^,²()

^1.蚌埠医科大学第一附属医院，检验科，安徽蚌埠 233000
^2.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 233000
^3.蚌埠医科大学检验医学院，安徽蚌埠 233000

收稿日期:2024-12-03 出版日期:2025-03-20 发布日期:2025-03-28
通讯作者: 李静 E-mail:lixiayin311@163.com;sdlj13409@163.com
作者简介:殷丽霞，在读硕士研究生，E-mail: lixiayin311@163.com
基金资助:
国家自然科学基金(81902078);安徽省高校优秀青年基金(2022AH030138);安徽省卫生健康委科研项目(AHWJ2022b088);安徽省教育厅优秀青年教师培育项目(YQYB2023019)

Cimifugin ameliorates Crohn's disease-like colitis in mice by modulating Th-cell immune balance via inhibiting the MAPK pathway

Lixia YIN¹^,³(), Minzhu NIU², Keni ZHANG¹^,³, Zhijun GENG², Jianguo HU¹^,², Jiangyan LI¹^,², Jing LI¹^,²()

^1.Department of Clinical Laboratory, Bengbu Medical University, Bengbu, 233000, China
^2.Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-Related Diseases, The First Affiliated Hospital of Bengbu Medical University, Bengbu, 233000, China, Bengbu Medical University, Bengbu, 233000, China
^3.College of Laboratory Medicine, Bengbu Medical University, Bengbu, 233000, China

Received:2024-12-03 Online:2025-03-20 Published:2025-03-28
Contact: Jing LI E-mail:lixiayin311@163.com;sdlj13409@163.com
Supported by:
National Natural Science Foundation of China(81902078)

摘要/Abstract

摘要：

目的探索升麻素（CIM）对小鼠克罗恩病（CD）样结肠炎的作用以及可能的机制。方法 30只体质量20~23 g（6~8周龄）的C57BL/6雄性小鼠随机分为空白对照组、2，4，6-三硝基苯磺酸（TNBS）组和CIM组，10只/组。TNBS组使用TNBS灌肠建立CD样结肠炎模型，CIM组经TNBS灌肠后每日灌胃CIM（12.5 mg/kg）。通过记录小鼠体质量变化和疾病活动指数（DAI）评分，测量结肠长度，进行HE染色炎症评分以及检测肠黏膜中炎症因子水平评估CIM对小鼠结肠炎的作用；采用免疫荧光及免疫印记检测小鼠肠屏障损伤；流式细胞术检测各组小鼠肠系膜淋巴结中辅助性T细胞亚群的比例；通过网络药理学预测CIM潜在作用靶点，KEGG富集分析筛选关键通路，分子对接验证CIM与MAPK通路核心蛋白的结合能力；Western blotting验证MAPK信号通路的改变。结果 CIM干预改善了TNBS诱导的小鼠体质量降低和结肠缩短，同时DAI评分和结肠组织炎症评分低于TNBS组（P<0.05）。ELISA和PCR检测结果显示，同TNBS组相比，CIM降低小鼠肠黏膜组织中促炎因子（IFN-γ和IL-17）的水平并促进抗炎因子（IL-4和IL-10）表达（P<0.05）。免疫荧光结果显示，CIM可改善TNBS诱导的小鼠上皮细胞Claudin-1的缺失和移位，以及杯状细胞的减少（P<0.05）；免疫印记数据提示CIM组小鼠结肠黏膜中Claudin-1和ZO-1表达高于TNBS组（P<0.05）。流式细胞术检测结果表明CIM干预后肠系膜淋巴结中Th1和Th17细胞比例下降，而Th2及Treg细胞比例升高（P<0.05）。KEGG富集分析发现CIM对肠炎的作用可能与MAPK信号通路相关，分子对接显示，CIM与MAPK通路核心靶点之间有很好的结合，免疫印记结果显示p-JNK、p-ERK和p-p38在CIM组的小鼠肠黏膜中表达低于TNBS组（P<0.05）。结论 CIM可改善肠屏障损伤从而缓解TNBS诱导的小鼠克罗恩病样结肠炎，这与其抑制MAPK信号通路的激活调节小鼠肠道Th1/Th2和Th17/Treg平衡有关。

关键词: 克罗恩病, 升麻素, MAPK, 辅助性T细胞, 免疫平衡, 肠屏障

Abstract:

Objective To investigate the therapeutic effects of cimifugin on Crohn's disease (CD)-like colitis in mice and its possible mechanism. Methods Thirty adult male C57BL/6 mice were randomized equally into control group, 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced CD-like colitis model group, and cimifugin treatment (daily gavage at 12.5 mg/kg) group. The therapeutic effect of cimifugin was evaluated by observing changes in body weight, disease activity index (DAI) scores, colon length, histopathological inflammation scores, and inflammatory cytokine levels in the colonic mucosa. Intestinal barrier integrity in the mice was assessed using immunofluorescence assay and Western blotting for claudin-1 and ZO-1; T-helper (Th) cell subset ratios in the mesenteric lymph nodes were analyzed with flow cytometry. Network pharmacology, KEGG enrichment analysis and molecular docking were used to predict the targets of cimifugin and analyze the key pathways and cimifugin-MAPK protein interactions, which were validated by Western blotting in the mouse models. Results In mice with TNBS-induced colitis, cimifugin treatment significantly attenuated body weight loss and colon shortening, lowered DAI and histopathological scores, decreased IFN-γ and IL-17 levels, and increased IL-4 and IL-10 levels in the colonic mucosa. Cimifugin treatment also significantly improved TNBS-induced claudin-1 dislocation and reduction of goblet cells, upregulated claudin-1 and ZO-1 expressions, reduced Th1 and Th17 cell percentages, and increased Th2 and Treg cell percentages in the colonic mucosa of the mice. KEGG analysis suggested a possible connection between the effect of cimifugin and MAPK signaling, and molecular docking showed strong binding affinity between cimifugin and MAPK core proteins. Western blotting demonstrated significantly decreased phosphorylation levels of JNK, ERK, and p38 in the colonic mucosa of cimifugin-treated mouse models. Conclusion Cimifugin alleviates TNBS-induced CD-like colitis by repairing intestinal barrier damage and restoring Th1/Th2 and Th17/Treg balance via suppressing MAPK pathway activation.

Key words: Crohn's disease, cimifugin, MAPK, helper T cells, immune homeostasis, intestinal barrier

殷丽霞, 牛民主, 张可妮, 耿志军, 胡建国, 李江艳, 李静. 升麻素抑制MAPK通路调节辅助性T细胞免疫平衡改善小鼠克罗恩病样结肠炎[J]. 南方医科大学学报, 2025, 45(3): 595-602.

Lixia YIN, Minzhu NIU, Keni ZHANG, Zhijun GENG, Jianguo HU, Jiangyan LI, Jing LI. Cimifugin ameliorates Crohn's disease-like colitis in mice by modulating Th-cell immune balance via inhibiting the MAPK pathway[J]. Journal of Southern Medical University, 2025, 45(3): 595-602.

图/表 10

表1 RT-qPCR的引物序列

Tab.1 Primer sequences for RT-qPCR

Gene	Primer sequences (5'-3')
IL-17A	F:GGCCCTCAGACTACCTCAAC
IL-17A	R:TCTCGACCCTGAAAGTGAAGG
IL-4	F:CCCCAGCTAGTTGTCATCCTG
IL-4	R:CAAGTGATTTTTGTCGCATCCG
IL-10	F:GCTGGACAACATACTGCTAACC
IL-10	R:ATTTCCGATAAGGCTTGGCAA
IFN-γ	F:ACAGCAAGGCGAAAAAGGATG
IFN-γ	R:TGGTGGACCACTCGGATGA
GAPDH	F:TGACCTCAACTACATGGTCTACA
GAPDH	R:CTTCCCATTCTCGGCCTTG

图1 CIM对小鼠实验性结肠炎症状的影响

Fig.1 Effect of cimifugin (CIM) on symptoms of TNBS-induced colitis in mice. A: Daily body weight changes of the mice in each group. B: Changes in DAI scores of the mice in each group. C: Gross observation of the mouse colon in each group. D: Comparison of colonic lengths of the mice among the 3 groups. *P<0.05 vs WT; #P<0.05 vs TNBS. WT: Type; TNBS: 2,4,6-trinitrobenzenesulfonic acid.

图2 CIM对小鼠实验性结肠炎肠组织损伤的影响

Fig.2 Effect of CIM on intestinal tissue damage in mice with TNBS-induced colitis. A: HE staining of mouse colon tissues. B: Inflammation scores of mouse colon tissue in each group. *P<0.05 vs WT; #P<0.05 vs TNBS.

图3 CIM对小鼠实验性结肠炎肠黏膜炎症状况的影响

Fig.3 Effect of CIM on intestinal mucosa inflammation of the mice in each group. A: Levels of inflammatory factors in the colonic mucosa detected by ELISA. B: mRNA expressions of inflammatory factors in the colonic mucosa detected by PCR. *P<0.05 vs WT; #P<0.05 vs TNBS.

图4 CIM对小鼠实验性结肠炎肠屏障损伤的影响

Fig.4 Effect of CIM on intestinal barrier damage in mice with TNBS-induced colitis. A: Immunofluorescence staining of claudin-1 in the colon of the mice in each group. B: AB-PAS staining of mouse colon. C: Numbers of goblet cells based on AB-PAS staining. D-F: Western blotting for detecting expression levels of ZO-1 and claudin-1 in colonic mucosal tissue. *P<0.05 vs WT; #P<0.05 vs TNBS.

图5 CIM对实验性结肠炎小鼠Th1/Th2细胞应答平衡的影响

Fig.5 Effect of CIM on balance of Th1/Th2 cell response in mice with TNBS-induced colitis. A, B: Assessment of Th1 cell percentage in mouse mesenteric lymph nodes by flow cytometry. C, D: Assessment of Th2 cell percentage in mouse mesenteric lymph nodes by flow cytometry. *P<0.05 vs WT; #P<0.05 vs TNBS.

图6 CIM对实验性结肠炎小鼠Th17/Treg细胞应答平衡的影响

Fig.6 Effect of CIM on balance of Th17/Treg cell response in mice with TNBS-induced colitis. A, B: Assessment of Th17 cell percentage in mouse mesenteric lymph nodes by flow cytometry. C, D: Assessment of Treg cell percentage in mouse mesenteric lymph nodes by flow cytometry. *P<0.05 vs WT; #P<0.05 vs TNBS.

图7 CIM网络药理学及分子对接

Fig.7 CIM network pharmacology and molecular docking. A:Venn diagram. B:PPI network diagram. C:KEGG analysis. D:GO analysis(CC, BP, MF).

表2 分子对接结果

Tab.2 Molecular docking results

Compound	Target	PDB	Energy (kcal/mol)
CIM	MAP3K14	8YHW	-8.4
CIM	MAP2K1	3EQI	-8.3
CIM	MAPK14	6SFO	-8.2
CIM	MAPK1	6SLG	-7.6
CIM	IKBKB	4KIK	-7.5
CIM	BRAF	5VYK	-6.7
CIM	CASP3	1RE1	-6.5
CIM	JUN	6Y3V	-5.7

图8 验证MAPK信号通路是否参与CIM改善小鼠实验性结肠炎

Fig.8 Verification of the role of the MAPK signaling pathway in mediating the therapeutic effect of CIM on TNBS-induced colitis in mice. A, B: Expressions of key proteins of the MAPK pathway (p-p38, p-ERK and p-JNK) detected in the intestinal mucosal tissues of the mice by Western blotting. *P<0.05 vs WT; #P<0.05 vs TNBS.

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升麻素抑制MAPK通路调节辅助性T细胞免疫平衡改善小鼠克罗恩病样结肠炎

Cimifugin ameliorates Crohn's disease-like colitis in mice by modulating Th-cell immune balance via inhibiting the MAPK pathway

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