pedunculoside and Inflammation

Mastitis is a disease that seriously threatens the health of the mammary gland after delivery. Pedunculoside (PE) is the main bioactive component of Aquifoliaceae. The purpose of this experiment is to explore the effects of PE on mastitis and its underlying mechanisms. Our research results showed that PE could significantly inhibit the increase in the levels of inflammatory mediators such as TNF-α, IL-6, IL-1β, MPO and iNOS during mastitis. Mechanism studies have found that PE could significantly inhibit the phosphorylation of AKT protein and binds to the ASP-184 site. Further research found that PE also inhibited the activation of AKT's downstream pro-inflammatory signals NF-κB and MAPK. In addition, PE effectively promote the expression of tight junction proteins occludin and claudin-3 during inflammation, maintaining the integrity of the blood-milk barrier. In summary, our research shows that PE inhibits the phosphorylation of AKT/NF-κB and MAPK signals; It also relieves mastitis by repairing the blood-milk barrier.

Topics: Animals; Female; Glucose; Inflammation; Inflammation Mediators; Lipopolysaccharides; Male; MAP Kinase Signaling System; Mastitis; Mice; NF-kappa B; Triterpenes

Pedunculoside (PE) is derived from the bark of iron holly, a member of the holly family. Previous studies have shown that PE has anti-inflammatory, antitumor, antiviral, cholesterol-lowering and blood-pressure-lowering effects. In this study, we aimed to investigate the effects of PE on ulcerative colitis and to explore its potential mechanisms. We treated a mouse model of ulcerative colitis induced by DSS (dextran sulfate sodium) with PE. The results showed that PE had an obvious effect on DSS-induced ulcerative colitis. PE significantly improved the colon length and clinical score in mice, and significantly inhibited the production of inflammatory cytokines. In the LPS-induced inflammatory response of RAW264.7 macrophages, we also found that PE significantly inhibited the phosphorylation of AKT, ERK1/2, JNK1/2, P65, and P38 to reduce the production of IL-1β, IL-6, TNF-α, COX-2, and iNOS. Furthermore, PE suppressed the LPS-induced transcriptional activities of nuclear factor P65 as well as the phosphorylation of P65. In addition, we also studied the effect of PE on LPS induced AKT/NF-κB and MAPK signaling pathways with primary peritoneal macrophages. In summary, PE has a beneficial effect on ulcerative colitis, and may be a potential natural product in the treatment of ulcerative colitis.

Topics: Animals; Cell Survival; Colitis, Ulcerative; Cytokines; Dextran Sulfate; Gene Expression Regulation; Glucose; Inflammation; Lipopolysaccharides; Macrophages; Male; Mice; Mice, Inbred C57BL; Molecular Structure; Random Allocation; RAW 264.7 Cells; Triterpenes