TY - JOUR
T1 - Apigenin supplementation protects the development of dextran sulfate sodium-induced murine experimental colitis by inhibiting canonical and non-canonical inflammasome signaling pathways
AU - Márquez-Flores, Yazmín K.
AU - Villegas, Isabel
AU - Cárdeno, Ana
AU - Rosillo, M. Ángeles
AU - Alarcón-de-la-Lastra, Catalina
N1 - Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/4/1
Y1 - 2016/4/1
N2 - The present study was designed to elucidate the protective effects of dietary apigenin (API) enrichment in a chronic colitis model induced by DSS in mice. Inflammatory mediators and the possible role of canonical and non-canonical NLRP3 inflammasome signaling pathways in the beneficial effects of API under chronic inflammatory conditions were also explored. Six-week-old mice were randomized in four dietary groups: sham and control groups received standard diet (SD), and other two groups were fed with API at 0.1%. After 30 days, all groups except sham received 3% DSS in drinking water for 5 days followed by a regime of 21 days of water. Our results revealed that dietary API supplementation decreased the macroscopic and microscopic damage signs of colitis; also, it was capable to down-regulate mPGES, COX-2 and iNOS enzyme colonic expressions and to decrease serum matrix metalloproteinase (MMP-3) levels. Similarly, API diet reduced IL-1β and TNF-α proinflammatory cytokine secretions in primary LPS-stimulated splenocytes. Furthermore, we demonstrated that API anti-inflammatory activity was related with an inhibition of both canonical and non-canonical NLRP3 inflammasome pathways by decreasing proinflammatory IL-1β and IL-18 cytokine levels as a consequence of regulation of cleaved caspase-1 and caspase-11 enzymes. We conclude that API supplement might provide a basis for developing a new dietary strategy for the prevention of chronic ulcerative colitis.
AB - The present study was designed to elucidate the protective effects of dietary apigenin (API) enrichment in a chronic colitis model induced by DSS in mice. Inflammatory mediators and the possible role of canonical and non-canonical NLRP3 inflammasome signaling pathways in the beneficial effects of API under chronic inflammatory conditions were also explored. Six-week-old mice were randomized in four dietary groups: sham and control groups received standard diet (SD), and other two groups were fed with API at 0.1%. After 30 days, all groups except sham received 3% DSS in drinking water for 5 days followed by a regime of 21 days of water. Our results revealed that dietary API supplementation decreased the macroscopic and microscopic damage signs of colitis; also, it was capable to down-regulate mPGES, COX-2 and iNOS enzyme colonic expressions and to decrease serum matrix metalloproteinase (MMP-3) levels. Similarly, API diet reduced IL-1β and TNF-α proinflammatory cytokine secretions in primary LPS-stimulated splenocytes. Furthermore, we demonstrated that API anti-inflammatory activity was related with an inhibition of both canonical and non-canonical NLRP3 inflammasome pathways by decreasing proinflammatory IL-1β and IL-18 cytokine levels as a consequence of regulation of cleaved caspase-1 and caspase-11 enzymes. We conclude that API supplement might provide a basis for developing a new dietary strategy for the prevention of chronic ulcerative colitis.
KW - Apigenin
KW - Caspases
KW - Chronic colitis
KW - DSS
KW - Inflammasome
UR - http://www.scopus.com/inward/record.url?scp=84962106536&partnerID=8YFLogxK
U2 - 10.1016/j.jnutbio.2015.12.002
DO - 10.1016/j.jnutbio.2015.12.002
M3 - Artículo
C2 - 27012631
SN - 0955-2863
VL - 30
SP - 143
EP - 152
JO - Journal of Nutritional Biochemistry
JF - Journal of Nutritional Biochemistry
ER -