Protective effects of Bee pollen extract on the Caco-2 intestinal barrier dysfunctions induced by dextran sulfate sodium

被引：36
作者：
Li, Qiangqiang [1 ]
Liang, Xinwen [1 ]
Guo, Nana [1 ]
Hu, Lin [2 ,3 ]
Prasad, Maruthi E. [4 ]
Wu, Yajun [5 ]
Xue, Xiaofeng [1 ]
Wu, Liming [1 ]
Wang, Kai [1 ]
机构：
[1] Chinese Acad Agr Sci, Inst Apicultural Res, Beijing 100093, Peoples R China
[2] Soochow Univ, Inst Biol, Suzhou 215123, Peoples R China
[3] Soochow Univ, Inst Med Sci, Suzhou 215123, Peoples R China
[4] Shenzhen Univ, Dept Cell Biol & Genet, Hlth Sci Ctr, Shenzhen 518060, Peoples R China
[5] Chinese Acad Inspect & Quarantine, Beijing 100176, Peoples R China
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2019年 / 117卷
基金：
中国国家自然科学基金;
关键词：
Bee pollen; Caco-2; cells; Intestinal barrier; Antioxidant and anti-inflammatory effects; Metabolomics; LIQUID-CHROMATOGRAPHY; INDUCED COLITIS; MECHANISMS; INTEGRITY; CELLS; MODEL;
D O I：
10.1016/j.biopha.2019.109200
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Bee pollen (BP) is a natural medicine from the hive with various potential health-promoting benefits, but until now there is no study to determine its protective roles in inflammatory bowel disease (IBD). The aim of this study was to reveal the in vitro gastrointestinal protective effects of BP against IBD using molecular and metabolic methods. Dextran sulfate sodium (DSS) challenged Caco-2 cell monolayers were applied to mimic intestinal epithelial cell dysfunctions and metabolic disorders. The pretreatment with BP extract rich in polyphenols ameliorated DSS-induced cell viability losses. It also exerted protective effects against intestinal barrier impairment by strengthening epithelial integrity and tight junction losses induced by DSS. BP up-regulated antioxidant (NQO1, Txnrd1, Nrf2) and down-regulated inflammatory (TNF-alpha and IL-6) mRNA expressions, in accompany with MAPK signaling inhibition. Furthermore, metabolomics analysis based on UPLC-Q-TOF/MS revealed that BP, and DSS treated Caco-2 cells have different metabolomic profiles, with significant changes on key metabolites involved in glycerophospholipid metabolism. Our results showed that BP has great therapeutic potential throughout the early stages of DSS-induced colitis.
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页数：10
相关论文
共 36 条
[21]   The Nrf2-Antioxidant Response Element Signaling Pathway and Its Activation by Oxidative Stress [J].
Nguyen, Truyen ;
Nioi, Paul ;
Pickett, Cecil B. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (20) :13291-13295
[22]   p38 MAPK mediates calcium oxalate crystal-induced tight junction disruption in distal renal tubular epithelial cells [J].
Peerapen, Paleerath ;
Thongboonkerd, Visith .
SCIENTIFIC REPORTS, 2013, 3
[23]   Cytokines induce tight junction disassembly in airway cells via an EGFR-dependent MAPK/ERK1/2-pathway [J].
Petecchia, Loredana ;
Sabatini, Federica ;
Usai, Cesare ;
Caci, Emanuela ;
Varesio, Luigi ;
Rossi, Giovanni A. .
LABORATORY INVESTIGATION, 2012, 92 (08) :1140-1148
[24]   Loss of the tight junction protein ZO-1 in dextran sulfate sodium induced colitis [J].
Poritz, Lisa S. ;
Garver, Kristian I. ;
Green, Cecelia ;
Fitzpatrick, Leo ;
Ruggiero, Francesca ;
Koltun, Walter A. .
JOURNAL OF SURGICAL RESEARCH, 2007, 140 (01) :12-19
[25]  
Prelipcean A. A., 2012, Cercetari Agronomice in Moldova, V45, P81
[26]   Metabolorn cs for phytomedicine research and drug development [J].
Shyur, Lie-Fen ;
Yang, Ning-Sun .
CURRENT OPINION IN CHEMICAL BIOLOGY, 2008, 12 (01) :66-71
[27]  
Solomon L., 2010, Comp. Clin. Path., V19, P235, DOI [10.1007/s00580-010-0979-4, DOI 10.1007/S00580-010-0979-4, :10.1007/s00580-010-0979-4]
[28]   TNFR2 Activates MLCK-Dependent Tight Junction Dysregulation to Cause Apoptosis-Mediated Barrier Loss and Experimental Colitis [J].
Su, Liping ;
Nalle, Sam C. ;
Shen, Le ;
Turner, Emily S. ;
Singh, Gurminder ;
Breskin, Lydia A. ;
Khramtsova, Ekaterina A. ;
Khramtsova, Galina ;
Tsai, Pei-Yun ;
Fu, Yang-Xin ;
Abraham, Clara ;
Turner, Jerrold R. .
GASTROENTEROLOGY, 2013, 145 (02) :407-415
[29]   Transforming growth factor-β1 is a new form of tumor suppressor with true haploid insufficiency [J].
Tang, BW ;
Böttinger, EP ;
Jakowlew, SB ;
Bagnall, KM ;
Mariano, J ;
Anver, MR ;
Letterio, JJ ;
Wakefield, LM .
NATURE MEDICINE, 1998, 4 (07) :802-807
[30]   Attenuated expression of the tight junction proteins is involved in clopidogrel-induced gastric injury through p38 MAPK activation [J].
Wu, Hai-Lu ;
Gao, Xin ;
Jang, Zong-Dan ;
Duan, Zhao-Tao ;
Wang, Shu-Kui ;
He, Bang-Shun ;
Zhang, Zhen-Yu ;
Xie, Hong-Guang .
TOXICOLOGY, 2013, 304 :41-48
1234