p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling

p-Hydroxybenzaldehyde (HD), the main active component of Nostoc commune, has been shown to attenuate dextran sulfate sodium (DSS)-induced experimental colitis. However, it is still unclear whether HD or its metabolites exert a protective role in ulcerative colitis (UC). In this study, we showed that...

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Autores principales: Xiaotian Xu, Ailin Luo, Xi Lu, Meng Liu, Huideng Wang, Hengzhi Song, Chengqiong Wei, Yuhui Wang, Xiaoqun Duan
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Publicado: Elsevier 2021
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spelling oai:doaj.org-article:d456aa801e654ef4a5fced13ef650a272021-11-10T04:21:49Zp-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling1756-464610.1016/j.jff.2021.104835https://doaj.org/article/d456aa801e654ef4a5fced13ef650a272021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1756464621004849https://doaj.org/toc/1756-4646p-Hydroxybenzaldehyde (HD), the main active component of Nostoc commune, has been shown to attenuate dextran sulfate sodium (DSS)-induced experimental colitis. However, it is still unclear whether HD or its metabolites exert a protective role in ulcerative colitis (UC). In this study, we showed that p-hydroxybenzoic acid (HA) is the active metabolite of HD and demonstrated the effects of HA in alleviating colitis and its potential mechanism. Mice with colitis induced by DSS were orally administered or intraperitoneally injected with therapeutic drugs (including HD, HA, mesalazine and PHTPP) for 10 days. Caco-2 cells were treated with TNF-α (10 ng/ml) and therapeutic drugs (including HA, mesalazine and PHTPP) for 24 h. The results showed that oral supplementation, but not intraperitoneal injection, of HD (40 mg/kg) significantly ameliorated DSS-induced colitis. Oral administration of HA (10-40 mg/kg) dose-dependently attenuated various colitis phenotypes in DSS-treated mice. Treatment with HA also decreased the expression of proinflammatory cytokines and increased the expression of tight junction proteins in mice and Caco-2 cells. However, combined treatment of HA with PHTPP, a highly selective antagonist of the estrogen receptor β (ERβ), did not show anti-colitis effects. Collectively, our results demonstrate that both HD and HA are active substances capable of inhibiting inflammatory responses and improving intestinal mucosal damage via the activation of ERβ signaling in DSS-induced colitis.Xiaotian XuAilin LuoXi LuMeng LiuHuideng WangHengzhi SongChengqiong WeiYuhui WangXiaoqun DuanElsevierarticleUlcerative colitisP-hydroxybenzoic acidInflammatory responseIntestinal mucosal damageEstrogen receptor βNutrition. Foods and food supplyTX341-641ENJournal of Functional Foods, Vol 87, Iss , Pp 104835- (2021)
institution DOAJ
collection DOAJ
language EN
topic Ulcerative colitis
P-hydroxybenzoic acid
Inflammatory response
Intestinal mucosal damage
Estrogen receptor β
Nutrition. Foods and food supply
TX341-641
spellingShingle Ulcerative colitis
P-hydroxybenzoic acid
Inflammatory response
Intestinal mucosal damage
Estrogen receptor β
Nutrition. Foods and food supply
TX341-641
Xiaotian Xu
Ailin Luo
Xi Lu
Meng Liu
Huideng Wang
Hengzhi Song
Chengqiong Wei
Yuhui Wang
Xiaoqun Duan
p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
description p-Hydroxybenzaldehyde (HD), the main active component of Nostoc commune, has been shown to attenuate dextran sulfate sodium (DSS)-induced experimental colitis. However, it is still unclear whether HD or its metabolites exert a protective role in ulcerative colitis (UC). In this study, we showed that p-hydroxybenzoic acid (HA) is the active metabolite of HD and demonstrated the effects of HA in alleviating colitis and its potential mechanism. Mice with colitis induced by DSS were orally administered or intraperitoneally injected with therapeutic drugs (including HD, HA, mesalazine and PHTPP) for 10 days. Caco-2 cells were treated with TNF-α (10 ng/ml) and therapeutic drugs (including HA, mesalazine and PHTPP) for 24 h. The results showed that oral supplementation, but not intraperitoneal injection, of HD (40 mg/kg) significantly ameliorated DSS-induced colitis. Oral administration of HA (10-40 mg/kg) dose-dependently attenuated various colitis phenotypes in DSS-treated mice. Treatment with HA also decreased the expression of proinflammatory cytokines and increased the expression of tight junction proteins in mice and Caco-2 cells. However, combined treatment of HA with PHTPP, a highly selective antagonist of the estrogen receptor β (ERβ), did not show anti-colitis effects. Collectively, our results demonstrate that both HD and HA are active substances capable of inhibiting inflammatory responses and improving intestinal mucosal damage via the activation of ERβ signaling in DSS-induced colitis.
format article
author Xiaotian Xu
Ailin Luo
Xi Lu
Meng Liu
Huideng Wang
Hengzhi Song
Chengqiong Wei
Yuhui Wang
Xiaoqun Duan
author_facet Xiaotian Xu
Ailin Luo
Xi Lu
Meng Liu
Huideng Wang
Hengzhi Song
Chengqiong Wei
Yuhui Wang
Xiaoqun Duan
author_sort Xiaotian Xu
title p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
title_short p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
title_full p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
title_fullStr p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
title_full_unstemmed p-Hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in DSS-induced colitis by activating ERβ signaling
title_sort p-hydroxybenzoic acid alleviates inflammatory responses and intestinal mucosal damage in dss-induced colitis by activating erβ signaling
publisher Elsevier
publishDate 2021
url https://doaj.org/article/d456aa801e654ef4a5fced13ef650a27
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