马鞭草苷通过抑制PI3K-AKT通路减轻肠上皮炎症改善小鼠克罗恩病样结肠炎

doi:10.12122/j.issn.1673-4254.2026.02.20

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (2): 423-433.doi: 10.12122/j.issn.1673-4254.2026.02.20

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马鞭草苷通过抑制PI3K-AKT通路减轻肠上皮炎症改善小鼠克罗恩病样结肠炎

黄林林¹(), 郑旺¹, 胡建国²^,⁴, 宋雪³^,⁴, 陶露³^,⁴, 耿志军³^,⁴, 李静²^,⁴, 左芦根¹^,⁴, 葛思堂¹^,⁴()

^1.蚌埠医科大学第一附属医院，胃肠外科，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.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

收稿日期:2025-06-09 出版日期:2026-02-20 发布日期:2026-03-10
通讯作者: 葛思堂 E-mail:huangl1nl1n@163.com;gesitang@163.com
作者简介:黄林林，在读硕士研究生，E-mail: huangl1nl1n@163.com
基金资助:
安徽省临床医学研究转化项目(202427b10020017);安徽高校自然科学研究项目(2024AH051222)

Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway

Linlin HUANG¹(), Wang ZHENG¹, Jianguo HU²^,⁴, Xue SONG³^,⁴, Lu TAO³^,⁴, Zhijun GENG³^,⁴, Jing LI²^,⁴, Lugen ZUO¹^,⁴, Sitang GE¹^,⁴()

^1.Department of Gastrointestinal Surgery, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China
^2.Department of 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.Anhui Key Laboratory of Basic and Translational Research on Inflammation-Related Diseases, Bengbu 233004, China

Received:2025-06-09 Online:2026-02-20 Published:2026-03-10
Contact: Sitang GE E-mail:huangl1nl1n@163.com;gesitang@163.com

摘要/Abstract

摘要：

目的探讨天然植物提取物马鞭草苷（VE）对克罗恩病（CD）样结肠炎的改善作用及其机制。方法建立2，4，6-三硝基苯磺酸（TNBS）诱导的小鼠结肠炎模型和脂多糖（LPS）刺激的结肠类器官损伤模型。将50只C57BL/6小鼠随机分为5组：WT组、TNBS组，VE低、中、高剂量组（5、10、20 mg/kg），10只/组。TNBS模型通过25 mg/L TNBS乙醇溶液灌肠建立，VE组每日腹腔注射相应剂量药物，连续治疗7 d。结肠类器官取自C57BL/6小鼠结肠隐窝，培养至第10天分为对照组、LPS组（100 μg/mL LPS处理24 h）和LPS+VE组（5、10、20 μmol/L VE共处理）。通过疾病活动指数（DAI）、结肠组织病理学评分、脾指数及炎症因子水平（IL-6、IL-1β、TNF-α）评估VE的疗效；采用免疫荧光染色、Western blotting检测紧密连接蛋白（ZO-1、Claudin-1）的表达；利用Western blotting检测PI3K-AKT通路蛋白的表达变化；结合PI3K-AKT通路激动剂740 Y-P干预实验验证通路调控机制。结果 VE缓解TNBS小鼠的结肠炎症状（降低DAI评分、结肠炎症评分及脾指数，缓解体质量下降和结肠缩短）（P<0.05），同时，VE干预可下调黏膜组织促炎因子（IL-6、IL-1β、TNF-α）的表达（P<0.05），上调ZO-1和Claudin-1蛋白表达（P<0.05），减少细菌移位（P<0.05）。机制上，VE可下调p-PI3K、p-AKT蛋白的表达（P<0.05），且其疗效可被PI3K-AKT激动剂（740 Y-P）逆转（P<0.05）。结论 VE通过调控PI3K-AKT信号通路抑制肠道炎症，从而修复肠屏障功能，改善小鼠CD样结肠炎。

关键词: 克罗恩病, 炎症性肠病, 肠屏障, PI3K-AKT, 马鞭草苷

Abstract:

Objective To investigate the therapeutic effect of verbenalin (VE) on Crohn's disease (CD)‑like colitis and the underlying molecular mechanism. Methods Fifty C57BL/6 mice were randomly divided into control group, TNBS group, and low-, medium-, and high-dose VE treatment groups (n=10). Mouse models of CD-like colitis were established in all but the control group by enema with 25 mg/L TNBS dissolved in ethanol, and the mice in VE treatment groups received daily intraperitoneal injections of VE at 5, 10, or 20 mg/kg for 7 days. Cultured colon organoids derived from mouse crypts were exposed to 100 μg/mL lipopolysaccharide (LPS) for 24 h and treated with 5, 10, or 20 μmol/L VE. The therapeutic effects of VE in the mouse models were evaluated by assessing changes in disease activity index (DAI), histopathological scores, and spleen index. In both colonic mucosa of the mouse models and the colon organoids, the levels of inflammatory cytokines, expressions of tight junction proteins, and changes in PI3K-AKT pathway proteins were analyzed, and the regulatory mechanism of VE was verified using the PI3K-AKT agonist 740 Y-P. Results In TNBS-treated mice, VE treatment significantly reduced DAI, histopathological scores, and spleen index, and mitigated weight loss, colon shortening and bacterial translocation. VE obviously lowered the expression of pro-inflammatory cytokines in colonic mucosa of the mice and the colon organoids, upregulated ZO-1 and claudin-1 expressions, and reduced bacterial translocation. VE significantly downregulated p-PI3K and p-AKT protein expressions, which was reversed by treatment with 740 Y-P. Conclusion VE inhibits intestinal inflammation and protects intestinal barrier function in mice with CD-like colitis by modulating the PI3K-AKT signaling pathway.

Key words: Crohn's disease, inflammatory bowel disease, intestinal barrier, PI3K-AKT, verbenalin

黄林林, 郑旺, 胡建国, 宋雪, 陶露, 耿志军, 李静, 左芦根, 葛思堂. 马鞭草苷通过抑制PI3K-AKT通路减轻肠上皮炎症改善小鼠克罗恩病样结肠炎[J]. 南方医科大学学报, 2026, 46(2): 423-433.

Linlin HUANG, Wang ZHENG, Jianguo HU, Xue SONG, Lu TAO, Zhijun GENG, Jing LI, Lugen ZUO, Sitang GE. Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway[J]. Journal of Southern Medical University, 2026, 46(2): 423-433.

图/表 8

表1 引物序列

Tab.1 Primer sequences for RT-qPCR

Gene	Primer sequence (5'to 3')
TNF-α	F: CACGCTCTTCTGTCTACTGAACTTC
TNF-α	R: CTTGGTGGTTTGTGAGTGTGAGG
IL-1β	F: AATCTCGCAGCAGCACATCAAC
IL-1β	R: AGGTCCACGGGAAAGACACAG
IL-6	F: GAGAGGAGACTTCACAGAGGATACC
IL-6	R: TCATTTCCACGATTTCCCAGAGAAC
GAPDH	F: AACTCCCACTCTTCCACCTTCG R: TCCACCACCCTGTTGCTGTAG

图1 VE干预对TNBS诱导的小鼠结肠炎症状的影响

Fig.1 Effects of VE treatment on TNBS-induced colitis symptoms in mice. A: Body weight changes. B: Disease activity index (DAI) scores. C: Spleen index. D: Spleen size. E: Gross morphology of mouse colon. F: Quantitative analysis of colon length. G: Histological inflammation score. H: HE staining of the colon tissue (n=10). *P<0.05.

图2 VE干预对小鼠肠屏障功能和结构的影响

Fig.2 Effects of VE on intestinal barrier function and structure in mice. A-D: Bacterial culture and translocation rates in the lymph nodes, liver, and spleen. E: Immunofluorescence staining of ZO-1 and claudin-1 in colonic mucosa. F-G: Western blotting bands and quantitative analysis of ZO-1 and claudin-1 protein expression (n=10). *P<0.05.

图3 VE干预对TNBS小鼠黏膜组织中的炎症介质水平的影响

Fig.3 Effects of VE on inflammatory mediator levels in colonic mucosa of TNBS-treated mice. A-C: ELISA detection of IL-6, IL-1β, and TNF-α protein levels. D-F: RT-qPCR analysis of IL-6, IL-1β, and TNF-α mRNA expression levels (n=10). *P<0.05.

图4 VE干预对LPS诱导的结肠类器官肠屏障损伤的影响

Fig.4 Effects of VE on LPS-induced intestinal barrier injury in colonic organoids. A: Immunofluorescence staining of ZO-1 and claudin-1. B: Microscopic images of colonic organoids. C: Quantitative analysis of organoid area. D-F: Western blotting for analysis of ZO-1 and claudin-1 protein expression levels (n=3). *P<0.05.

图5 VE干预对LPS诱导结肠类器官的炎症介质水平的影响

Fig.5 Effects of VE on inflammatory mediator levels in LPS-induced colonic organoids. A-C: ELISA detection of IL-6, IL-1β, and TNF-α protein levels. D-F: RT-qPCR analysis of IL-6, IL-1β, and TNF-α mRNA expression levels (n=3). *P<0.05.

图6 VE干预对PI3K-AKT的信号通路活化的影响

Fig.6 Effects of VE on PI3K-AKT signaling pathway activation. A, B: Western blotting for analysis of p-PI3K/PI3K and p-AKT/AKT protein expressions in colon tissues of TNBS-treated mice (n=10). C, D: Western blotting for analysis of p-PI3K/PI3K and p-AKT/AKT protein expressions in LPS-induced colonic organoids (n=3). *P<0.05.

图7 VE通过抑制PI3K-AKT信号通路来影响小鼠克罗恩病样结肠炎

Fig.7 VE ameliorates colitis in mice by inhibiting the PI3K-AKT signaling pathway. A: DAI scores following 740 Y-P intervention. B: Histological inflammation scores. C: HE staining of the colon tissue. D-E: mRNA and protein expression levels of IL-6, IL-1β, and TNF-α in the colonic mucosa. n=10, *P<0.05.

参考文献 38

[1]	Wong SY, Estevinho MM, Heaney T, et al. Goblet cell loss linked to NOD2 and secondary resection in Crohn's disease is induced by dysbiosis and epithelial MyD88[J]. Cell Mol Gastroenterol Hepatol, 2025: 101533. doi：10.1016/j.jcmgh.2025.101533
[2]	Palmela C, Chevarin C, Xu ZL, et al. Adherent-invasive Escherichia coli in inflammatory bowel disease[J]. Gut, 2018, 67(3): 574-87. doi：10.1136/gutjnl-2017-314903
[3]	Liang WJ, Zhang W, Tian JY, et al. Advances in carbohydrate-based nanoparticles for targeted therapy of inflammatory bowel diseases: a review[J]. Int J Biol Macromol, 2024, 281(Pt 4): 136392. doi：10.1016/j.ijbiomac.2024.136392
[4]	Pinelli M, Makdissi S, Scur M, et al. Peroxisomal cholesterol metabolism regulates Yap-signaling, which maintains intestinal epithelial barrier function and is altered in Crohn’s disease[J]. Cell Death Dis, 2024, 15(7): 536. doi：10.1038/s41419-024-06925-x
[5]	李静, 孙洋, 熊心雨, 等. 樱黄素抑制TLR4/MyD88通路减轻肠上皮炎症反应改善小鼠克罗恩病样结肠炎[J]. 细胞与分子免疫学杂志, 2024, 40(3): 199-206.
[6]	Ma WY, Wang M, Chen JK, et al. Qingshu Yiqi decoction ameliorates exertional heat stroke-induced intestinal barrier injury via NF‑κB/MLC pathway and gut microbiota[J]. Phytomedicine, 2025, 143: 156723. doi：10.1016/j.phymed.2025.156723
[7]	Kim HM, Kim YM. HMGB1: LPS delivery vehicle for caspase-11-mediated pyroptosis[J]. Immunity, 2018, 49(4): 582-4. doi：10.1016/j.immuni.2018.09.021
[8]	Veloso PM, Machado R, Nobre C. Mesalazine and inflammatory bowel disease-From well-established therapies to progress beyond the state of the art[J]. Eur J Pharm Biopharm, 2021, 167: 89-103. doi：10.1016/j.ejpb.2021.07.014
[9]	Kapizioni C, Desoki R, Lam D, et al. Biologic therapy for inflammatory bowel disease: real-world comparative effectiveness and impact of drug sequencing in 13 222 patients within the UK IBD BioResource[J]. J Crohns Colitis, 2024, 18(6): 790-800.
[10]	Alajmi A, Yuan YH, Solitano V, et al. 5-Aminosalicylates for non-surgical patients with active or quiescent Crohn's disease: an overview of systematic reviews (umbrella review)[J]. J Crohns Colitis, 2025, 19(5): jjaf069. doi：10.1093/ecco-jcc/jjaf069
[11]	李艳, 刘阳, 郑敏, 等. 苍苓止泻口服液治疗儿童腹泻的系统评价[J]. 中国医院用药评价与分析, 2018, 18(1): 74-7, 82.
[12]	朱鸿全. 桃红马鞭汤治疗子宫内膜异位症48例[J]. 陕西中医, 1998, 19(12): 532.
[13]	赵益人. 马鞭草合剂治疗血尿[J]. 上海中医药杂志, 1979, 13(4): 26.
[14]	Wang YY, Wang X, Li YX, et al. Xuanfei Baidu Decoction reduces acute lung injury by regulating infiltration of neutrophils and macrophages via PD-1/IL17A pathway[J]. Pharmacol Res, 2022, 176: 106083. doi：10.1016/j.phrs.2022.106083
[15]	Kang ZC, Jiang WL, Luan HY, et al. Cornin induces angiogenesis through PI3K-Akt-ENOS-VEGF signaling pathway[J]. Food Chem Toxicol, 2013, 58: 340-6. doi：10.1016/j.fct.2013.05.017
[16]	Dong JH, Du CL, Xu CT, et al. Verbenalin attenuates hepatic damage and mitochondrial dysfunction in alcohol-associated steatohepatitis by regulating MDMX/PPARα‑mediated ferroptosis[J]. J Ethnopharmacol, 2023, 307: 116227. doi：10.1016/j.jep.2023.116227
[17]	Zuo LG, Li J, Zhang XF, et al. Aberrant mesenteric adipose extracellular matrix remodelling is involved in adipocyte dysfunction in Crohn's disease: the role of TLR-4-mediated macrophages[J]. J Crohns Colitis, 2022, 16(11): 1762-76. doi：10.1093/ecco-jcc/jjac087
[18]	Lukonin I, Serra D, Challet Meylan L, et al. Phenotypic landscape of intestinal organoid regeneration[J]. Nature, 2020, 586(7828): 275-80. doi：10.1038/s41586-020-2776-9
[19]	Alula KM, Dowdell AS, LeBere B, et al. Interplay of gut microbiota and host epithelial mitochondrial dysfunction is necessary for the development of spontaneous intestinal inflammation in mice[J]. Microbiome, 2023, 11(1): 256. doi：10.1186/s40168-023-01686-9
[20]	Zuo LG, Li J, Ge ST, et al. Bryostatin-1 ameliorated experimental colitis in Il-10^-/- Mice by protecting the intestinal barrier and limiting immune dysfunction[J]. J Cell Mol Med, 2019, 23(8): 5588-99. doi：10.1111/jcmm.14457
[21]	李晴晴, 黄菊, 孙洋, 等. 乙酰紫堇灵通过抑制肠上皮细胞凋亡改善三硝基苯磺酸诱导的小鼠克罗恩病样结肠炎[J]. 南方医科大学学报, 2023, 43(8): 1306-14.
[22]	Li YY, Wang XJ, Su YL, et al. Baicalein ameliorates ulcerative colitis by improving intestinal epithelial barrier via AhR/IL-22 pathway in ILC3s[J]. Acta Pharmacol Sin, 2022, 43(6): 1495-507. doi：10.1038/s41401-021-00781-7
[23]	Dönder Y, Arikan TB, Baykan M, et al. Effects of quercitrin on bacterial translocation in a rat model of experimental colitis[J]. Asian J Surg, 2018, 41(6): 543-50. doi：10.1016/j.asjsur.2017.12.002
[24]	Zuo LG, Geng ZJ, Song X, et al. Browning of mesenteric white adipose tissue in Crohn’s disease: a new pathological change and therapeutic target[J]. J Crohns Colitis, 2023, 17(8): 1179-92. doi：10.1093/ecco-jcc/jjad046
[25]	Wirtz S, Popp V, Kindermann M, et al. Chemically induced mouse models of acute and chronic intestinal inflammation[J]. Nat Protoc, 2017, 12(7): 1295-309. doi：10.1038/nprot.2017.044
[26]	Wei ZY, Ni X, Cui H, et al. Engeletin attenuates the inflammatory response via inhibiting TLR4-NFκB signaling pathway in Crohn's disease-like colitis[J]. J Ethnopharmacol, 2025, 336: 118733. doi：10.1016/j.jep.2024.118733
[27]	Gao ZX, Yu XC, Su WL, et al. Atractylenolide-1 alleviates ulcerative colitis via restraining RhoA/ROCK/MLC pathway-mediated intestinal barrier dysfunction[J]. J Agric Food Chem, 2025, 73(21): 12690-701. doi：10.1021/acs.jafc.4c11976
[28]	Liu HY, Li SC, Ogamune KJ, et al. Probiotic Lactobacillus johnsonii reduces intestinal inflammation and rebalances splenic treg/Th17 responses in dextran sulfate sodium-induced colitis[J]. Antioxidants (Basel), 2025, 14(4): 433. doi：10.3390/antiox14040433
[29]	Leibovitzh H, Lee SH, Xue MY, et al. Altered gut microbiome composition and function are associated with gut barrier dysfunction in healthy relatives of patients with Crohn's disease[J]. Gastroenterology, 2022, 163(5): 1364-76.e10. doi：10.1053/j.gastro.2022.07.004
[30]	Sato Y, Kanayama M, Nakajima S, et al. Sialyllactose enhances the short-chain fatty acid production and barrier function of gut epithelial cells via nonbifidogenic modification of the fecal microbiome in human adults[J]. Microorganisms, 2024, 12(2): 252. doi：10.3390/microorganisms12020252
[31]	Spalinger MR, Schwarzfischer M, Niechcial A, et al. Loss of PTPN22 promotes intestinal inflammation by compromising granulocyte-mediated antibacterial defence[J]. J Crohns Colitis, 2021, 15(12): 2118-30. doi：10.1093/ecco-jcc/jjab098
[32]	Hazime H, Ducasa GM, Santander AM, et al. DUOX2 activation drives bacterial translocation and subclinical inflammation in IBD-associated dysbiosis[J]. Gut, 2025, 74(10): 1589-601. doi：10.1136/gutjnl-2024-334346
[33]	Zhang J, Zhao LL, He JY, et al. Protect effects of Perilla seed extract and its active ingredient luteolin against inflammatory bowel disease model via the PI3K/AKT signal pathway in vivo and in vitro [J]. Int J Mol Sci, 2025, 26(8): 3564. doi：10.3390/ijms26083564
[34]	Qiao M, Xue TT, Zhu Y, et al. Polysaccharides from Cistanche deserticola mitigate inflammatory bowel disease via modulating intestinal microbiota and SRC/EGFR/PI3K/AKT signaling pathways[J]. Int J Biol Macromol, 2025, 308(Pt 2): 142452. doi：10.1016/j.ijbiomac.2025.142452
[35]	Zhang SF, Zhong RQ, Zhou M, et al. Mechanisms of baicalin alleviates intestinal inflammation: role of M1 macrophage polarization and Lactobacillus amylovorus [J]. Adv Sci (Weinh), 2025, 12(21): e2415948. doi：10.1002/advs.202415948
[36]	Geng ZJ, Zuo LG, Li J, et al. Ginkgetin improved experimental colitis by inhibiting intestinal epithelial cell apoptosis through EGFR/PI3K/AKT signaling[J]. FASEB J, 2024, 38(14): e23817. doi：10.1096/fj.202400211rr
[37]	Hu JY, Niu JJ, Jiang SS, et al. Qilian Jiechang Ning alleviates TNBS-induced ulcerative colitis in mice and segatella copri outer membrane vesicle-triggered inflammation in colon epithelial cells via the caspase-1/11-GSDMD pathways[J]. J Innate Immun, 2025, 17(1): 262-76. doi：10.1159/000545394
[38]	Zhao HM, Xu R, Huang XY, et al. Curcumin improves regulatory T cells in gut-associated lymphoid tissue of colitis mice[J]. World J Gastroenterol, 2016, 22(23): 5374-83. doi：10.3748/wjg.v22.i23.5374

马鞭草苷通过抑制PI3K-AKT通路减轻肠上皮炎症改善小鼠克罗恩病样结肠炎

Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway

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