咖啡酸乙酯通过激活Wnt/β-Catenin通路恢复肠上皮紧密连接缓解小鼠结肠炎

doi:10.12122/j.issn.1673-4254.2026.09.18

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (9): 2196-2205.doi: 10.12122/j.issn.1673-4254.2026.09.18

• • 上一篇

咖啡酸乙酯通过激活Wnt/β-Catenin通路恢复肠上皮紧密连接缓解小鼠结肠炎

张可妮¹(), 张龙涛¹, 章雨¹, 黄菊², 李晴晴¹, 耿志军², 胡建国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 233004
^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 233004

收稿日期:2026-01-22 出版日期:2026-09-20 发布日期:2026-09-30
通讯作者: 李静 E-mail:kenizhang0906@163.com;lijingbyfy@bbmu.edu.cn
作者简介:张可妮，在读硕士研究生，E-mail: kenizhang0906@163.com
基金资助:
安徽省临床医学研究转化专项(202427b10020088);炎症相关性疾病基础与转化研究安徽省重点实验室开放课题(YZ2025B04);炎症相关性疾病基础与转化研究安徽省重点实验室开放课题(YZ2025B03);蚌埠医科大学研究生创新计划项目(Byycx25018)

Ethyl caffeate alleviates dextran sulfate sodium-induced colitis in mice by restoring intestinal epithelial tight junctions via activating the Wnt/β-Catenin pathway

Keni ZHANG¹(), Longtao ZHANG¹, Yu ZHANG¹, Ju HUANG², Qingqing LI¹, Zhijun GENG², Jianguo HU¹^,², Jing LI¹^,²()

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

Received:2026-01-22 Online:2026-09-20 Published:2026-09-30
Contact: Jing LI E-mail:kenizhang0906@163.com;lijingbyfy@bbmu.edu.cn

摘要/Abstract

摘要：

目的探讨咖啡酸乙酯（EC）调控肠屏障对葡聚糖硫酸钠（DSS）诱导小鼠结肠炎的作用和机制。方法将40只SPF级C57BL/6雄性小鼠随机分为对照组、DSS模型组（DSS）及3个不同剂量的EC干预组（5、10、20 mg/kg），共5组，8只/组。通过自由饮用2.5% DSS构建结肠炎模型，造模同时每日灌胃给予相应剂量EC，持续干预7 d。通过体质量变化、疾病活动指数（DAI）、结肠长度及组织病理学评分结果，系统评估结肠炎表型；免疫荧光检测紧密连接蛋白ZO-1、Claudin-1的表达与定位；AB-PAS染色评估杯状细胞数量；ELISA、RT-qPCR及免疫组化检测炎症水平；采用网络药理学预测EC调控的关键信号通路并采用Western blotting和信号通路抑制剂分析其作用机制。结果 EC（10 mg/kg）可显著缓解DSS诱导的结肠炎症状：与DSS组相比，EC组体质量下降减少，DAI评分降低，结肠长度恢复，结肠组织病理损伤减轻（均P<0.05）。进一步检测发现EC显著下调肠黏膜组织中炎症因子TNF-α、IL-6的mRNA及蛋白表达，降低肠黏膜MPO阳性水平（P<0.05）；EC对DSS诱导肠屏障损伤亦有显著的改善作用，不仅可恢复杯状细胞数量，还可上调紧密连接蛋白ZO-1/Claudin-1的表达并恢复其细胞膜定位（P<0.05）。网络药理学筛选出350个EC与炎症性肠病（IBD）的交集基因，KEGG富集分析发现Wnt/β-catenin及紧密连接为EC的核心作用通路。Western blotting检测结果显示，EC可激活DSS诱导的肠上皮细胞中Wnt/β-catenin通路，上调WNT3A及β-catenin表达（P<0.05）；采用Wnt通路抑制剂IWR-1干预可阻断EC对紧密连接蛋白及Wnt/β-catenin通路的上调和激活作用。结论咖啡酸乙酯通过激活Wnt/β-catenin信号通路，促进肠上皮紧密连接蛋白的表达，改善肠黏膜屏障功能并缓解DSS诱导的小鼠结肠炎，为炎症性肠病的天然化合物干预提供新的候选药物及作用靶点。

关键词: 咖啡酸乙酯, 炎症性肠病, Wnt/β-catenin通路, 肠上皮紧密连接, 肠黏膜屏障, 杯状细胞

Abstract:

Objective To observe the effect of ethyl caffeate (EC) on intestinal barrier function in mice with dextran sulfate sodium (DSS)-induced murine colitis and explore the possible mechanism. Methods Forty male C57BL/6 mice were randomized into control group, DSS model group, and 3 EC groups treated with EC at 5, 10, or 20 mg/kg. Mouse models of colitis were established bytreatment with 2.5% DSS for 7 days, and EC treatment was administered daily by gavage. Colitis phenotypes were assessed by changes in body weight, disease activity index (DAI), colon length and histology. Immunofluorescence staining and PAS staining were used to examine the changes in expressions of the tight junction proteins ZO-1 and claudin-1 and goblet cells, respectively. The intestinal levels of inflammatory factors were detected by ELISA, RT-qPCR and immunohistochemistry. Network pharmacology combined with Western blotting and Wnt inhibitor (IWR-1) was used to verify the mechanism of EC for ameliorating colitis. Results Treatment with EC at 10 mg/kg significantly alleviated DSS-induced colitis in the mouse models, reduced intestinal pro-inflammatory cytokines and MPO levels, increased goblet cell counts, and restored ZO-1 and claudin-1 expressions and their membrane localization. Network pharmacology identified Wnt/β‑catenin and tight junction pathways as the core targets of EC, which activated the Wnt/β‑catenin pathway by upregulating WNT3A/β‑catenin, and this effect was blocked by treatment with IWR-1. Conclusion EC ameliorates DSS-induced colitis in mice by activating Wnt/β‑catenin signaling to restore tight junction protein expressions and localization, thereby improving intestinal barrier function, suggesting the value of EC as a novel candidate for treatment of inflammatory bowel disease.

Key words: Ethyl Caffeate, inflammatory bowel disease, Wnt/β-Catenin pathway, intestinal epithelial tight junctions, intestinal mucosal barrier, goblet cells

张可妮, 张龙涛, 章雨, 黄菊, 李晴晴, 耿志军, 胡建国, 李静. 咖啡酸乙酯通过激活Wnt/β-Catenin通路恢复肠上皮紧密连接缓解小鼠结肠炎[J]. 南方医科大学学报, 2026, 46(9): 2196-2205.

Keni ZHANG, Longtao ZHANG, Yu ZHANG, Ju HUANG, Qingqing LI, Zhijun GENG, Jianguo HU, Jing LI. Ethyl caffeate alleviates dextran sulfate sodium-induced colitis in mice by restoring intestinal epithelial tight junctions via activating the Wnt/β-Catenin pathway[J]. Journal of Southern Medical University, 2026, 46(9): 2196-2205.

图/表 10

表1 引物序列

Tab.1 Primer sequences for RT-qPCR

Gene name	Gene ID	Primer sequences (5'-3')
IL-6	16193	F:TCTATACCACTTCACAAGTCGGA
		R:GAATTGCCATTGCACAACTCTTT
TNF-α	21926	F:CAGGCGGTGCCTATGTCTC
		R:CGATCACCCCGAAGTTCAGTAG
ZO-1	21872	F: TTCACAGAGCAGCGACAACT
		R: TCTGCTGGAGTAGGCTACGA
Claudin-1	100771737	F: AAAGCACCGGGCAGATACAA
		R: TCATGCCAATGGTGGACACA
GAPDH	14433	F:TGGCCTTCCGTGTTCCTAC
		R:GAGTTGCTGTTGAAGTCGCA

图1 EC干预可减轻DSS诱导的小鼠结肠炎症状

Fig.1 Ethyl caffeate (EC) alleviates dextran sulfate sodium (DSS)-induced colitis symptoms in mice. A: Body weight alterations in mice from the Control, DSS model, EC-5 mg/kg, EC-10 mg/kg, and EC-20 mg/kg groups. B: Disease activity index (DAI) scores of the 5 groups. C: Representative colonic images of the mice. D: Mouse colon length measurements (cm). *P<0.05 vs Control; #P<0.05 vs DSS.

图2 EC减轻结肠组织病理损伤并抑制炎症水平

Fig.2 EC attenuates colonic pathology and inflammation in mice with DSS-induced colitis. A: Histological analysis and inflammation scoring of mouse colons using HE staining. B: MPO immunohistochemistry and the average optical density (AOD) in the 3 groups. C: TNF‑α and IL‑6 protein concentrations in colonic mucosa quantified using ELISA. D: Relative mRNA expression of TNF‑α and IL‑6 in colonic mucosa measured by RT‑qPCR. *P<0.05 vs Control; #P<0.05 vs DSS.

图3 EC改善DSS诱导小鼠肠屏障损伤

Fig.3 EC improves DSS-induced intestinal barrier dysfunction. A: AB-PAS staining of mouse colon and goblet cell counts. B: Claudin-1 expression (immunohistochemical staining) and the average optical density (AOD). *P<0.05 vs Control; #P<0.05 vs DSS.

图4 EC上调肠黏膜紧密连接分子表达

Fig.4 EC upregulates expression of intestinal mucosal tight junction proteins. A: Western blotting of ZO-1 and claudin-1 expression in colonic mucosal tissues. B: Relative mRNA expression levels of ZO-1 and claudin-1 in colonic mucosa determined by RT-qPCR. *P<0.05 vs Control; #P<0.05 vs DSS.

图5 网络药理学筛选

Fig.5 Network pharmacology of EC. A: Venn map. B: PPI network C: KEGG pathway enrichment. D: GO functional annotation (BP, CC, MF).

图6 EC对Caco-2细胞无明显毒性

Fig.6 EC exhibits no obvious cytotoxicity in Caco-2 cells. *P<0.05 vs EC=0 μmol/L.

图7 EC改善DSS诱导的Caco-2细胞屏障结构紊乱

Fig.7 EC improves DSS-induced barrier structure disorder in Caco-2 cells. A: Relative mRNA expression levels of ZO-1 and claudin-1 in Caco-2 cells detected by RT-qPCR. B: Western blotting of ZO-1 and claudin-1 protein expressions in Caco-2 cells. C: Immunofluorescence staining of ZO-1 (red) and claudin-1 (green) localization and fluorescence intensity in Caco-2 cells. *P<0.05 vs Control; #P<0.05 vs DSS.

图8 EC可激活Wnt/β-catenin通路

Fig.8 EC activates the Wnt/β-catenin signaling pathway in DSS-induced Caco-2 cells. *P<0.05 vs Control; #P<0.05 vs DSS.

图9 EC修复肠上皮屏障的效应依赖Wnt/β-catenin通路

Fig.9 EC depend on the Wnt/β-catenin pathway to promote repair of intestinal epithelial barrier function. *P<0.05 vs DSS+EC.

参考文献 36

[1]	Kaplan GG. The global burden of IBD: from 2015 to 2025[J]. Nat Rev Gastroenterol Hepatol, 2015, 12(12): 720-7. doi：10.1038/nrgastro.2015.150
[2]	Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease[J]. Nature, 2007, 448(7152): 427-34. doi：10.1038/nature06005
[3]	McLemore LJ. Inflammatory bowel disease[J]. Radiol Technol, 2007, 78(4): 291-305;quiz306-8.
[4]	Sairenji T, Collins KL, Evans DV. An update on inflammatory bowel disease[J]. Prim Care Clin Off Pract, 2017, 44(4): 673-92. doi：10.1016/j.pop.2017.07.010
[5]	Geremia A, Biancheri P, Allan P, et al. Innate and adaptive immunity in inflammatory bowel disease[J]. Autoimmun Rev, 2014, 13(1): 3-10. doi：10.1016/j.autrev.2013.06.004
[6]	Graham DB, Xavier RJ. Pathway paradigms revealed from the genetics of inflammatory bowel disease[J]. Nature, 2020, 578(7796): 527-39. doi：10.1038/s41586-020-2025-2
[7]	Söderholm JD, Olaison G, Peterson KH, et al. Augmented increase in tight junction permeability by luminal stimuli in the non-inflamed ileum of Crohn's disease[J]. Gut, 2002, 50(3): 307-13. doi：10.1136/gut.50.3.307
[8]	Martel J, Chang SH, Ko YF, et al. Gut barrier disruption and chronic disease[J]. Trends Endocrinol Metab, 2022, 33(4): 247-65. doi：10.1016/j.tem.2022.01.002
[9]	Li LL, Cheng R, Wu YS, et al. Diagnosis and management of inflammatory bowel disease[J]. J Evid Based Med, 2024, 17(2): 409-33. doi：10.1111/jebm.12626
[10]	Peng X, Zhong R, Dong S, et al. 18β‑Glycyrrhetinic acid from Glycyrrhiza Uralensis protects colonic epithelium in ulcerative colitis by activating Wnt/β-catenin pathway to restore tight junction[J]. Phytomedicine, 2025, 143: 156830. doi：10.1016/j.phymed.2025.156830
[11]	Degirmenci B, Valenta T, Dimitrieva S, et al. GLI1-expressing mesenchymal cells form the essential Wnt-secreting niche for colon stem cells[J]. Nature, 2018, 558(7710): 449-53. doi：10.1038/s41586-018-0190-3
[12]	Kuo WT, Zuo L, Odenwald MA, et al. The tight junction protein ZO-1 is dispensable for barrier function but critical for effective mucosal repair[J]. Gastroenterology, 2021, 161(6): 1924-39. doi：10.1053/j.gastro.2021.08.047
[13]	Chen C, Lin XH, Xie YM, et al. Shengjiang Xiexin Decoction ameliorates DSS-induced ulcerative colitis via activating Wnt/ β‑catenin signaling to enhance epithelium renovation and modulating intestinal flora[J]. Phytomedicine, 2025, 139: 156456. doi：10.1016/j.phymed.2025.156456
[14]	Zheng MY, Han R, Yuan YL, et al. The role of Akkermansia muciniphila in inflammatory bowel disease: Current knowledge and perspectives[J]. Front Immunol, 2023, 13: 1089600. doi：10.3389/fimmu.2022.1089600
[15]	高中良, 张丽英, 李梦青, 等. 牵牛子中咖啡酸和咖啡酸乙酯的提取研究[J]. 安徽农业科学, 2009, 37(7): 3049-50. doi：10.3969/j.issn.0517-6611.2009.07.088
[16]	Chiang YM, Chuang DY, Wang SY, et al. Metabolite profiling and chemopreventive bioactivity of plant extracts from Bidens pilosa [J]. J Ethnopharmacol, 2004, 95(2/3): 409-19. doi：10.1016/j.jep.2004.08.010
[17]	Chiang YM, Lo CP, Chen YP, et al. Ethyl caffeate suppresses NF-κB activation and its downstream inflammatory mediators, iNOS, COX-2, and PGE2in vitro or in mouse skin[J]. Br J Pharmacol, 2005, 146(3): 352-63. doi：10.1038/sj.bjp.0706343
[18]	廖余琼, 张妮, 刘翰飞, 等. 黔产硬毛夏枯草中1个新的松香烷型二萜化合物及其抗神经炎活性研究[J]. 中草药, 2025, 56(16): 5723-30.
[19]	Widodo A, Huang HT, Dewi NR, et al. Ethyl caffeate modulates systemic and mucosal immune responses, growth performance, and disease resistance against Vibrio parahaemolyticus in hybrid grouper (Epinephelus fuscoguttatus ♀ × E. lanceolatus ♂)[J]. Fish Shellfish Immunol, 2025, 158: 110163. doi：10.1016/j.fsi.2025.110163
[20]	Nguyen PT, Nakamura Y, Tran NQV, et al. Ethyl caffeate can inhibit aryl hydrocarbon receptor (AhR) signaling and AhR-mediated potentiation of mast cell activation[J]. Int J Mol Sci, 2023, 24(12): 9997. doi：10.3390/ijms24129997
[21]	Wang H, Song DZ, Wei LH, et al. Ethyl caffeate inhibits macrophage polarization via SIRT1/NF‑κB to attenuate traumatic heterotopic ossification in mice[J]. Biomed Pharmacother, 2023, 161: 114508. doi：10.1016/j.biopha.2023.114508
[22]	Shen JN, Xu LX, Shan L, et al. Neuroprotection of (+)-2-(1-hydroxyl-4-oxocyclohexyl) ethyl caffeate against hydrogen peroxide and lipopolysaccharide induced injury via modulating arachidonic acid network and p38-MAPK signaling[J]. Curr Alzheimer Res, 2015, 12(9): 892-902. doi：10.2174/156720501209151019111244
[23]	Huang YL, Li G, Li D, et al. Ethyl caffeate alleviates inflammatory response and promotes recovery in septic-acute lung injury via the TNF-α/NF-κB/MMP9 Axis[J]. Phytomedicine, 2025, 141: 156700. doi：10.1016/j.phymed.2025.156700
[24]	Mi YH, Zhong L, Lu SJ, et al. Quercetin promotes cutaneous wound healing in mice through Wnt/β‑catenin signaling pathway[J]. J Ethnopharmacol, 2022, 290: 115066. doi：10.1016/j.jep.2022.115066
[25]	Murthy SN, Cooper HS, Shim H, et al. Treatment of dextran sulfate sodium-induced murine colitis by intracolonic cyclosporin[J]. Dig Dis Sci, 1993, 38(9): 1722-34. doi：10.1007/bf01303184
[26]	张敏, 刘生宝, 张诺, 等. 改进型“瑞士卷”法在小鼠肠道组织切片中的应用[J]. 中华病理学杂志, 2024, 53(4): 393-7. doi：10.3760/cma.j.cn112151-20231016-00270
[27]	Schultz M, Tonkonogy SL, Sellon RK, et al. IL-2-deficient mice raised under germfree conditions develop delayed mild focal intestinal inflammation[J]. Am J Physiol, 1999, 276(6): G1461-72. doi：10.1152/ajpgi.1999.276.6.g1461
[28]	Xu CX, Huang XL, Deng ZC, et al. Dendrobium Officinale-derived carbon dots nanozymes alleviate colitis by orchestrating intestinal mucus-epithelium-immune barriers[J]. Adv Sci, 2025, 12(44): e12567. doi：10.1002/advs.202512567
[29]	Ye M, Fan MH, Zhao Y, et al. Low molecular weight Astragalus membranaceus polysaccharides alleviates dextran sulfate sodium-induced colitis in mice[J]. Carbohydr Polym, 2025, 367: 124050. doi：10.1016/j.carbpol.2025.124050
[30]	Le DD, Dang T, Truong V, et al. Integrative discovery through network pharmacology and molecular docking approaches of phenolic compounds isolated from Torreya nucifera to treat rheumatoid arthritis[J]. Int J Mol Sci, 2025, 26(23): 11629. doi：10.3390/ijms262311629
[31]	Ge ST, Yang YT, Zuo LG, et al. Sotetsuflavone ameliorates Crohn's disease-like colitis by inhibiting M1 macrophage-induced intestinal barrier damage via JNK and MAPK signalling[J]. Eur J Pharmacol, 2023, 940: 175464. doi：10.1016/j.ejphar.2022.175464
[32]	Oka A, Sartor RB. Microbial-based and microbial-targeted therapies for inflammatory bowel diseases[J]. Dig Dis Sci, 2020, 65(3): 757-88. doi：10.1007/s10620-020-06090-z
[33]	Li JW, Niu CX, Ai HH, et al. TSP50 attenuates DSS-induced colitis by regulating TGF‑β signaling mediated maintenance of intestinal mucosal barrier integrity[J]. Adv Sci, 2024, 11(11): 2305893. doi：10.1002/advs.202305893
[34]	Bland J. The gut mucosal firewall and functional medicine[J]. Integr Med, 2016, 15(4): 19-22.
[35]	Wei QZ, Jiang HX, Zeng J, et al. Quercetin protected the gut barrier in ulcerative colitis by activating aryl hydrocarbon receptor[J]. Phytomedicine, 2025, 140: 156633. doi：10.1016/j.phymed.2025.156633
[36]	Liang J, Dai WG, Liu CH, et al. Gingerenone a attenuates ulcerative colitis via targeting IL-17RA to inhibit inflammation and restore intestinal barrier function[J]. Adv Sci, 2024, 11(28): 2400206. doi：10.1002/advs.202400206

咖啡酸乙酯通过激活Wnt/β-Catenin通路恢复肠上皮紧密连接缓解小鼠结肠炎

Ethyl caffeate alleviates dextran sulfate sodium-induced colitis in mice by restoring intestinal epithelial tight junctions via activating the Wnt/β-Catenin pathway

RichHTML

PDF

可视化

摘要/Abstract

引用本文

使用本文

图/表 10

参考文献 36

相关文章 14

编辑推荐

Metrics

本文评价

[1]	张龙涛, 章雨, 乔通, 张可妮, 尹林, 黄菊, 李静, 耿志军, 胡建国. 丁香酸甲酯通过抑制MAPK通路调控肠上皮细胞凋亡减轻葡聚糖硫酸钠诱导的小鼠结肠炎[J]. 南方医科大学学报, 2026, 46(7): 1685-1695.
[2]	尹林, 章雨, 张可妮, 乔通, 张龙涛, 黄菊, 李静, 胡建国, 耿志军. 1，3-二咖啡酰奎宁酸通过抑制PI3K/Akt通路减轻氧化应激缓解葡聚糖硫酸钠诱导的小鼠结肠炎[J]. 南方医科大学学报, 2026, 46(6): 1244-1255.
[3]	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.
[4]	尹林, 张可妮, 乔通, 牛民主, 殷丽霞, 刘馨悦, 耿志军, 李静, 胡建国. 藜芦酸通过激活Nrf2/HO-1信号通路减轻氧化应激缓解葡聚糖硫酸钠诱导的小鼠实验性结肠炎[J]. 南方医科大学学报, 2026, 46(2): 403-411.
[5]	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.
[6]	储菲, 陈孝华, 宋博文, 杨晶晶, 左芦根. 苏荠宁黄酮通过抑制PI3K/AKT信号通路拮抗肠上皮细胞凋亡改善小鼠实验性结肠炎[J]. 南方医科大学学报, 2025, 45(4): 819-828.
[7]	陶露, 陈悦, 黄林林, 郑旺, 宋雪, 项平, 胡建国. 珠子草素通过调控p38/JNK信号通路抑制肠上皮细胞凋亡保护肠屏障改善克罗恩病样肠炎[J]. 南方医科大学学报, 2025, 45(11): 2483-2495.
[8]	邵荣瑢, 杨子, 张文静, 张诺, 赵雅静, 张小凤, 左芦根, 葛思堂. 茯苓酸缓解小鼠克罗恩病：基于抑制PI3K/AKT信号通路拮抗肠上皮细胞凋亡[J]. 南方医科大学学报, 2023, 43(6): 935-942.
[9]	肖姝喆, 成燕玲, 朱云, 唐芮, 古建标, 兰林, 何志华, 刘丹琼, 耿岚岚, 程旸, 龚四堂. WNT2b高表达的成纤维细胞破坏肠道黏膜屏障[J]. 南方医科大学学报, 2023, 43(2): 206-212.
[10]	戴世学，顾红祥，武钢，钟涛，菅洪健，湛永乐，张旻海，高勇，徐俊，陈东升，廖广捷，封艳玲，刘洪波，邹颖，迟宏罡. CD8+CD28+/CD8+CD28- T细胞平衡预测炎症性肠病患者并发消化道出血的价值[J]. 南方医科大学学报, 2016, 36(12): 1609-.
[11]	周有连，陈烨. 英夫利昔单抗治疗炎症性肠病的疗效及影响因素分析[J]. 南方医科大学学报, 2013, 33(12): 1833-.
[12]	张婷，陈烨，王中秋，周有连，张绍衡，王浦，谢珊，姜泊. 炎症性肠病患者肠道菌群结构的变化及其与炎性指标的关系[J]. 南方医科大学学报, 2013, 33(10): 1474-.
[13]	张朝霞，赵芯梅，吕超蓝，李晨，智发朝. 膜联蛋白A2在炎症性肠病肠粘膜中的表达及临床意义[J]. 南方医科大学学报, 2012, 32(11): 1548-.
[14]	简燕婷¹, 王继德¹, 麦国丰², 张亚历¹, 赖卓胜¹. 姜黄素对模型大鼠肠粘膜炎症因子的调控[J]. 南方医科大学学报, 2004, 24(12): 1353-1358.