AIM:To investigate the anti-inflammatory effects of cinnamon extract and elucidate its mechanisms for targeting the function of antigen presenting cells.METHODS:Cinnamon extract was used to treat murine macrophage cel...AIM:To investigate the anti-inflammatory effects of cinnamon extract and elucidate its mechanisms for targeting the function of antigen presenting cells.METHODS:Cinnamon extract was used to treat murine macrophage cell line(Raw 264.7),mouse primary antigen-presenting cells(APCs,MHCII+) and CD11c+dendritic cells to analyze the effects of cinnamon extract on APC function.The mechanisms of action of cinnamon extract on APCs were investigated by analyzing cytokine production,and expression of MHC antigens and co-stimulatory molecules by quantitative real-time PCR and flow cytometry.In addition,the effect of cinnamon extract on antigen presentation capacity and APC-dependent T-cell differentiation were analyzed by [H3]-thymidine incorporation and cytokine analysis,respectively.To confirm the anti-inflammatory effects of cinnamon extract in vivo,cinnamon or PBS was orally administered to mice for 20 d followed by induction of experimental colitis with 2,4,6 trinitrobenzenesulfonic acid.The protective effects of cinnamon extract against experimental colitis were measured by checking clinical symptoms,histological analysis and cytokine expression prof iles in inflamed tissue.RESULTS:Treatment with cinnamon extract inhibited maturation of MHCII+ APCs or CD11c+ dendritic cells(DCs) by suppressing expression of co-stimulatory molecules(B7.1,B7.2,ICOS-L),MHCII and cyclooxygenase(COX)-2.Cinnamon extract induced regulatory DCs(rDCs) that produce low levels of pro-inflammatory cytokines [interleukin(IL)-1β,IL-6,IL-12,interferon(IFN)-γ and tumor necrosis factor(TNF)-α] while expressing high levels of immunoregulatory cytokines(IL-10 and transforming growth factor-β).In addition,rDCs generated by cinnamon extract inhibited APC-dependent T-cell proliferation,and converted CD4+ T cells into IL-10high CD4+ T cells.Furthermore,oral administration of cinnamon extract inhibited development and progression of intestinal colitis by inhibiting expression of COX-2 and pro-inflammatory cytokines(IL-1β,IFN-γ and TNF-α),while enhancing IL-10 levels.CONCLUSION:Our study suggests the potential of cinnamon extract as an anti-inflammatory agent by targeting the generation of regulatory APCs and IL-10+ regulatory T cells.展开更多
Cinnamon is a traditional herbal medicine that is a valuable source of bioactive phenolic compounds.In this study,we determined the effects of cinnamon free phenolic extract(CFPE)on glucose transport in Caco-2 cells a...Cinnamon is a traditional herbal medicine that is a valuable source of bioactive phenolic compounds.In this study,we determined the effects of cinnamon free phenolic extract(CFPE)on glucose transport in Caco-2 cells and its possible mechanisms of action.First,the contents of phenolic compounds and flavonoids in bark were compared among four cinnamon cultivars.The‘Taiwan’cultivar had the highest contents of these compounds,and the CFPE was prepared from it.A Caco-2 monolayer was established,and the effect of CFPE on glucose transport across the monolayer was determined.The results showed that CFPE(at 150-300μg/mL)suppressed glucose transport across the monolayer in a dose-dependent manner.Procyanidin C1,procyanidin B2,procyanidin B1,procyanidin B3,procyanidin A2,and()-epicatechin derivatives in CFPE may have contributed to its suppressive effect.Treatment with CFPE decreased the transcript levels of SGK1 encoding serum and glucocorticoid-inducible kinase and PLC/PKC encoding phospholipase C/protein kinase C,which are involved in the signaling pathway associated with glucose transport;and the transcript levels of SGLT1 encoding sodium/glucose cotransporter 1 and GLUT2 encoding glucose transporter 2,the key glucose transporters in this pathway.These findings suggest that CFPE inhibits glucose transport via its effects on the signaling pathway and glucose transporters involved in glucose absorption in intestinal cells.Thus,CFPE has potential applications in preventing postprandial hyperglycemia.展开更多
基金Supported by Grants from the BioGreen 21 Program, Rural Development Administration (PJ007054)Regional Technology Innovation Program of the MOCIE (RTI05-01-01)Korea Healthcare Technology R&D Project, Ministry of Health and Welfare (A080588-20)
文摘AIM:To investigate the anti-inflammatory effects of cinnamon extract and elucidate its mechanisms for targeting the function of antigen presenting cells.METHODS:Cinnamon extract was used to treat murine macrophage cell line(Raw 264.7),mouse primary antigen-presenting cells(APCs,MHCII+) and CD11c+dendritic cells to analyze the effects of cinnamon extract on APC function.The mechanisms of action of cinnamon extract on APCs were investigated by analyzing cytokine production,and expression of MHC antigens and co-stimulatory molecules by quantitative real-time PCR and flow cytometry.In addition,the effect of cinnamon extract on antigen presentation capacity and APC-dependent T-cell differentiation were analyzed by [H3]-thymidine incorporation and cytokine analysis,respectively.To confirm the anti-inflammatory effects of cinnamon extract in vivo,cinnamon or PBS was orally administered to mice for 20 d followed by induction of experimental colitis with 2,4,6 trinitrobenzenesulfonic acid.The protective effects of cinnamon extract against experimental colitis were measured by checking clinical symptoms,histological analysis and cytokine expression prof iles in inflamed tissue.RESULTS:Treatment with cinnamon extract inhibited maturation of MHCII+ APCs or CD11c+ dendritic cells(DCs) by suppressing expression of co-stimulatory molecules(B7.1,B7.2,ICOS-L),MHCII and cyclooxygenase(COX)-2.Cinnamon extract induced regulatory DCs(rDCs) that produce low levels of pro-inflammatory cytokines [interleukin(IL)-1β,IL-6,IL-12,interferon(IFN)-γ and tumor necrosis factor(TNF)-α] while expressing high levels of immunoregulatory cytokines(IL-10 and transforming growth factor-β).In addition,rDCs generated by cinnamon extract inhibited APC-dependent T-cell proliferation,and converted CD4+ T cells into IL-10high CD4+ T cells.Furthermore,oral administration of cinnamon extract inhibited development and progression of intestinal colitis by inhibiting expression of COX-2 and pro-inflammatory cytokines(IL-1β,IFN-γ and TNF-α),while enhancing IL-10 levels.CONCLUSION:Our study suggests the potential of cinnamon extract as an anti-inflammatory agent by targeting the generation of regulatory APCs and IL-10+ regulatory T cells.
基金We acknowledge the Agricultural Competitive Industry Discipline Team Building Project of Guangdong Academy of Agricultural Sciences(202119TD)the Excellent Doctors Foundation of Guangdong Academy of Agricultural Sciences(R2021YJ-YB1002)+1 种基金the Guidance for Young Scientist of Guangdong Academy of Agricultural Sciences(R2020QD-043)the Innovative Research Team Construction Project for Modern Agricultural Industry Common Key Technologies of Guangdong Province(2022KJ117)for financial support.
文摘Cinnamon is a traditional herbal medicine that is a valuable source of bioactive phenolic compounds.In this study,we determined the effects of cinnamon free phenolic extract(CFPE)on glucose transport in Caco-2 cells and its possible mechanisms of action.First,the contents of phenolic compounds and flavonoids in bark were compared among four cinnamon cultivars.The‘Taiwan’cultivar had the highest contents of these compounds,and the CFPE was prepared from it.A Caco-2 monolayer was established,and the effect of CFPE on glucose transport across the monolayer was determined.The results showed that CFPE(at 150-300μg/mL)suppressed glucose transport across the monolayer in a dose-dependent manner.Procyanidin C1,procyanidin B2,procyanidin B1,procyanidin B3,procyanidin A2,and()-epicatechin derivatives in CFPE may have contributed to its suppressive effect.Treatment with CFPE decreased the transcript levels of SGK1 encoding serum and glucocorticoid-inducible kinase and PLC/PKC encoding phospholipase C/protein kinase C,which are involved in the signaling pathway associated with glucose transport;and the transcript levels of SGLT1 encoding sodium/glucose cotransporter 1 and GLUT2 encoding glucose transporter 2,the key glucose transporters in this pathway.These findings suggest that CFPE inhibits glucose transport via its effects on the signaling pathway and glucose transporters involved in glucose absorption in intestinal cells.Thus,CFPE has potential applications in preventing postprandial hyperglycemia.