Abstract
Background: The prevalence of inflammatory bowel disease is rapidly increasing around the world. Quercetin is a flavonoid commonly found in vegetables and fruits and has been reported to exert numerous pharmacological activities such as enhancing antioxidant capacity or suppressing inflammation.
Objective: We aimed to explore whether quercetin was effective for IBD and the underlying mechanism of quercetin for the ameliorative effects on the DSS-induced colitis in mice.
Methods: Thirty-six mice were randomly assigned to three treatments, including the control group (Ctr), DSS-induced colitis group (DSS) and DSS-induced colitis supplemented with 500 ppm quercetin (DQ500). Colitis was induced by DSS intake, and body weight was recorded every day. After six days administration of DSS, intestinal permeability was measured, and the liver was taken for antioxidant enzyme tests. Colonic tissue was taken for the histopathlogical score and RNA-sequencing analysis.
Results: In this experiment, dietary quercetin for 500ppm alleviated the DSS-induced colitis, possibly by strengthening intestinal integrity, liver antioxidant capacity. Based on the results of the transcriptome of colon tissue, several key genes were modulated by quercetin. ERK1/2-FKBP pathway and RXR-STAT3 pathway were involved in the development of IBD, furthermore, in the down-regulation of S100a8/9, FBN2 contributed to lowering the risk of colongenesis.
Conclusion: We demonstrated that dietary quercetin alleviated the DSS-induced colitis in mice. This is most likely due to its beneficial effects on intestinal integrity and modulation of several key pathways. Based on our research, quercetin was a promising candidate for IBD and its pharmaceutical effects on both IBD and colongenesis need further research.
Keywords: Colitis, quercetin, intestinal integrity, antioxidant, transcriptome, ERK1/2.
Graphical Abstract
[http://dx.doi.org/10.1038/nprot.2017.044] [PMID: 28569761]
[http://dx.doi.org/10.1053/j.gastro.2011.10.001] [PMID: 22001864]
[http://dx.doi.org/10.1016/j.asjsur.2017.12.002] [PMID: 29371051]
[http://dx.doi.org/10.1136/gut.2009.197822] [PMID: 20442201]
[http://dx.doi.org/10.1002/ibd.22926] [PMID: 22374887]
[http://dx.doi.org/10.1016/j.biopha.2019.109683 PMID: 31810123]
[http://dx.doi.org/10.3390/ijms161125942] [PMID: 26540040]
[http://dx.doi.org/10.1016/j.jff.2017.10.047]
[http://dx.doi.org/10.1016/j.redox.2016.08.012] [PMID: 27572418]
[http://dx.doi.org/10.18632/oncotarget.12415] [PMID: 27716626]
[http://dx.doi.org/10.3109/13880200490893492]
[http://dx.doi.org/10.1016/j.jnutbio.2013.02.007] [PMID: 23643524]
[http://dx.doi.org/10.4103/1319-3767.173753] [PMID: 26831601]
[http://dx.doi.org/10.1016/j.jfda.2014.06.011] [PMID: 28911485]
[http://dx.doi.org/10.1016/j.ejphar.2008.03.008] [PMID: 18417116]
[http://dx.doi.org/10.1016/j.chom.2017.05.009] [PMID: 28618266]
[http://dx.doi.org/10.1016/j.jff.2013.02.008]
[http://dx.doi.org/10.3389/fmicb.2019.01092] [PMID: 31156598]
[http://dx.doi.org/10.1080/15376516.2017.1351507 PMID: 28679351]
[http://dx.doi.org/10.1016/j.lfs.2013.01.028] [PMID: 23399699]
[http://dx.doi.org/10.1111/1440-1681.12894] [PMID: 29164668]
[http://dx.doi.org/10.3892/ijmm.2013.1317] [PMID: 23546389]
[http://dx.doi.org/10.3164/jcbn.16-109] [PMID: 28751803]
[http://dx.doi.org/10.1186/s12929-018-0419-3] [PMID: 29540173]
[http://dx.doi.org/10.1016/j.tiv.2007.03.005] [PMID: 17467952]
[http://dx.doi.org/10.1007/s10620-015-3528-9] [PMID: 25596721]
[http://dx.doi.org/10.1155/2008/586721] [PMID: 18776587]
[http://dx.doi.org/10.1007/s10620-010-1494-9] [PMID: 21203903]
[http://dx.doi.org/10.1038/s41467-019-09375-8]
[http://dx.doi.org/10.1155/2018/3271617]