Inflammatory bowel disease(IBD)is the consequence of a complex interplay between environmental factors,like dietary habits,that alter intestinal microbiota in response to luminal antigens in genetically susceptible in...Inflammatory bowel disease(IBD)is the consequence of a complex interplay between environmental factors,like dietary habits,that alter intestinal microbiota in response to luminal antigens in genetically susceptible individuals.Epigenetics represents an auspicious area for the discovery of how environmental factors influence the pathogenesis of inflammation,prognosis,and response to therapy.Consequently,it relates to gene expression control in response to environmental influences.The increasing number of patients with IBD globally is indicative of the negative effects of a food supply rich in trans and saturated fats,refined su-gars,starches and additives,as well as other environmental factors like seden-tarism and excess bodyweight,influencing the promotion of gene expression and increasing DNA hypomethylation in IBD.As many genetic variants are now associated with Crohn's disease(CD),new therapeutic strategies targeting modi-fiable environmental triggers,such as the implementation of an anti-inflammatory diet that involves the removal of potential food antigens,are of growing interest in the current literature.Diet,as a strong epigenetic factor in the pathogenesis of inflammatory disorders like IBD,provides novel insights into the pathophysio-logy of intestinal and extraintestinal inflammatory disorders.展开更多
OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect mi...OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect millions of adults worldwide.METHODS:In the present study,rats were fed with a high-fat-diet(HFD)with vitamin D3 for 16 weeks and were orally administered atorvastatin treatment and different doses of JPQT.Histopathological changes and ultrastructural changes in the aorta were evaluated through hematoxylin-eosin staining and transmission electron microscopy(TEM),respectively.Suppressor of cytokine signaling 1(SOCS1)/Janus kinase 1(JAK1)/signal transducer and activator of transcription 1(STAT1)signaling pathways were detected through Western blotting.RESULTS:JPQT treatment decreased the lipid levels of triglyceride,low-density lipoprotein,and cholesterol,the inflammatory cytokine levels of interleukin 1 beta(IL-1β),IL-6 and IL-8 in rat serum,but increased high-density lipoprotein and IL-10 serum levels.JPQT treatment ameliorated pathological changes in the aorta of AS model rats.Moreover,JPQT upregulated SOCS1 protein expression and down-regulated phosphorylated protein expression levels of p-JAK1 and p-STAT1.CONCLUSION:These results suggest that JPQT induces anti-atherosclerosis effects through anti-inflammatory and inhibiting JAK/STAT signaling pathways in HFD fed rats.展开更多
文摘Inflammatory bowel disease(IBD)is the consequence of a complex interplay between environmental factors,like dietary habits,that alter intestinal microbiota in response to luminal antigens in genetically susceptible individuals.Epigenetics represents an auspicious area for the discovery of how environmental factors influence the pathogenesis of inflammation,prognosis,and response to therapy.Consequently,it relates to gene expression control in response to environmental influences.The increasing number of patients with IBD globally is indicative of the negative effects of a food supply rich in trans and saturated fats,refined su-gars,starches and additives,as well as other environmental factors like seden-tarism and excess bodyweight,influencing the promotion of gene expression and increasing DNA hypomethylation in IBD.As many genetic variants are now associated with Crohn's disease(CD),new therapeutic strategies targeting modi-fiable environmental triggers,such as the implementation of an anti-inflammatory diet that involves the removal of potential food antigens,are of growing interest in the current literature.Diet,as a strong epigenetic factor in the pathogenesis of inflammatory disorders like IBD,provides novel insights into the pathophysio-logy of intestinal and extraintestinal inflammatory disorders.
基金the National Natural Science Foundation of China:Explore the Regulatory Mechanism of Coronary Endothelial Immune Inflammation Mediated by Micro RNA155-SOCS1 Axis in Bama Pigs based on “Xin Shou Qi Yu Pi”(No.81703970)the National 973 Program on Key Basic Research Project:Study on the Therapeutic Mechanism and Rule of Treating Angina Pectoris based on “Cong Pi Lun Zhi”(No.2013CB531704)
文摘OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect millions of adults worldwide.METHODS:In the present study,rats were fed with a high-fat-diet(HFD)with vitamin D3 for 16 weeks and were orally administered atorvastatin treatment and different doses of JPQT.Histopathological changes and ultrastructural changes in the aorta were evaluated through hematoxylin-eosin staining and transmission electron microscopy(TEM),respectively.Suppressor of cytokine signaling 1(SOCS1)/Janus kinase 1(JAK1)/signal transducer and activator of transcription 1(STAT1)signaling pathways were detected through Western blotting.RESULTS:JPQT treatment decreased the lipid levels of triglyceride,low-density lipoprotein,and cholesterol,the inflammatory cytokine levels of interleukin 1 beta(IL-1β),IL-6 and IL-8 in rat serum,but increased high-density lipoprotein and IL-10 serum levels.JPQT treatment ameliorated pathological changes in the aorta of AS model rats.Moreover,JPQT upregulated SOCS1 protein expression and down-regulated phosphorylated protein expression levels of p-JAK1 and p-STAT1.CONCLUSION:These results suggest that JPQT induces anti-atherosclerosis effects through anti-inflammatory and inhibiting JAK/STAT signaling pathways in HFD fed rats.
