peoniflorin and Colitis--Ulcerative
peoniflorin has been researched along with Colitis--Ulcerative* in 5 studies
Reviews
1 review(s) available for peoniflorin and Colitis--Ulcerative
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Paeoniflorin promotes intestinal stem cell-mediated epithelial regeneration and repair via PI3K-AKT-mTOR signalling in ulcerative colitis.
Ulcerative colitis (UC) is a chronic and immune-mediated inflammatory disorder characterized by abdominal pain, diarrhoea, and haematochezia. The goal of clinical therapy for UC is mucosal healing, accomplished by regenerating and repairing the intestinal epithelium. Paeoniflorin (PF) is a natural ingredient extracted from Paeonia lactiflora that has significant anti-inflammatory and immunoregulatory efficacy. In this study, we investigated how PF could regulate the renewal and differentiation of intestinal stem cells (ISCs) to improve the regeneration and repair of the intestinal epithelium in UC. Our experimental results showed that PF significantly alleviated colitis induced by dextran sulfate sodium (DSS) and ameliorated intestinal mucosal injury by regulating the renewal and differentiation of ISCs. The mechanism by which PF regulates ISCs was confirmed to be through PI3K-AKT-mTOR signalling. In vitro, we found that PF not only improved the growth of TNF-α-induced colon organoids but also increased the expression of genes and proteins related to the differentiation and regeneration of ISCs. Furthermore, PF promoted the repair ability of lipopolysaccharide (LPS)-induced IEC-6 cells. The mechanism by which PF regulates ISCs was further confirmed and was consistent with the in vivo results. Overall, these findings demonstrate that PF accelerates epithelial regeneration and repair by promoting the renewal and differentiation of ISCs, suggesting that PF treatment may be beneficial to mucosal healing in UC patients. Topics: Animals; Colitis; Colitis, Ulcerative; Dextran Sulfate; Disease Models, Animal; Humans; Intestinal Mucosa; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Regeneration; Stem Cells; TOR Serine-Threonine Kinases | 2023 |
Other Studies
4 other study(ies) available for peoniflorin and Colitis--Ulcerative
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Paeoniflorin ameliorates experimental colitis by inhibiting gram-positive bacteria-dependent MDP-NOD2 pathway.
Previous studies reported that antibiotics inhibit the growth of Gram-positive bacteria and alleviate ulcerative colitis (UC). But how Gram-positive bacteria are involved in the occurrence of inflammatory bowel disease (IBD) and which component of it causes inflammation remain unclear. This work aims to demonstrate that Gram-positive bacteria may be an underlying cause of experimental colitis in mice through the muramyl dipeptide (MDP)-nucleotide-binding oligomerization domain-containing protein-2 (NOD2) pathway and paeoniflorin inhibits the pathway above to alleviate experimental colitis. In this study, colitis mice were established by oral administration of 3% dextran sulfate sodium (DSS) and paeoniflorin (25, 50,100 mg/kg per day, ig) was administered to the mice for 10 days. Results shown that the abundance and the infiltration of Gram-positive bacteria in intestinal tissues increased in UC mice. Paeoniflorin treatment significantly alleviated DSS-induced experimental colitis mice, reduced the abundance of Gram-positive bacteria in feces and the infiltration of Gram-positive bacteria in intestinal tissues. Paeoniflorin also inhibited mRNA and protein expression of MDP-NOD2 pathway components and decreased the levels of related inflammatory cytokines. In vitro experiments showed that MDP strongly stimulated RAW264.7 cells to secrete tumor necrosis factor α (TNF-α), and induced translocation of nuclear factor-kappa B (NF-κB p65) from the cytoplasm to nucleus using immunofluorescence co-localization experiments. Overall, the results indicated that Gram-positive bacteria promote the occurrence of colitis via up-regulation of MDP-NOD2 pathway, and paeoniflorin is able to decrease the infiltration of Gram-positive bacteria in intestine and inhibit Gram-positive bacteria-dependent MDP-NOD2 pathway to alleviate mice colitis. Topics: Acetylmuramyl-Alanyl-Isoglutamine; Animals; Colitis, Ulcerative; Dextran Sulfate; Feces; Glucosides; Gram-Positive Bacteria; Intestines; Male; Mice; Mice, Inbred C57BL; Monoterpenes; Nod2 Signaling Adaptor Protein; RAW 264.7 Cells; RNA, Messenger; Signal Transduction; Transcription Factor RelA; Tumor Necrosis Factor-alpha | 2021 |
Paeoniflorin protects against dextran sulfate sodium (DSS)-induced colitis in mice through inhibition of inflammation and eosinophil infiltration.
Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that causes inflammation and ulcers in the digestive tract. The treatment commonly includes anti-inflammatory agents like 5-aminosalicylic acid or corticosteroids or biologics for people with UC who are no longer responding to corticosteroids. The radices of Paeonia lactiflora Pall. or similar plants of the Paeonia genus have been used in Chinese medicine to treat certain diseases that resemble the symptoms of UC. Paeoniflorin, a terpenoid glycoside, is a major active component for the anti-inflammatory and antitumor activity. In this study, we evaluated the therapeutic effect of paeoniflorin (PF) against dextran sulfate sodium (DSS)-induced colitis in mice and found that PF exhibited protective activity against colitis. PF treatment suppressed NF-κB pathway activation, resulting down regulation of pro-inflammatory factor expression. In addition, we detected reduction in eosinophil-related chemokine gene expression and eosinophil infiltration. The treatment also reversed Treg cell population suppression. Although PF treatment did not block COX2 induction, the compound weakly inhibited COX2 activity in an enzymatic assay. Taken together, PF exerts its therapeutic activity against UC through inhibition of inflammation and eosinophil infiltration. Topics: Animals; Anti-Inflammatory Agents; Colitis, Ulcerative; Colon; Dextran Sulfate; Disease Models, Animal; Eosinophils; Female; Glucosides; Humans; Intestinal Mucosa; Mice; Monoterpenes; Paeonia; Signal Transduction | 2021 |
[Paeoniflorin attenuates dextran sulfate sodium-induced ulcerative colitis in mice by inhibiting TLR5 expression and T cell activation].
Objective To investigate the therapeutic effect and mechanism of paeoniflorin on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) mice. Methods C57BL/6 male mice were randomly divided into control group, model group, 600 mg/(kg.d) mesalazine treatment group, (12.5, 25, 50) mg/(kg.d) paeoniflorin treatment group, with 10 mice in each. All mice were treated with 30 g/L DSS for 5 days except the control group. Meanwhile, the mice in the other groups were orally administrated corresponding drugs for 10 days, while the mice in the control and model groups were given equivalent volumes of distilled water. Body mass, fecal characteristics and hematochezia of the mice were observed and recorded daily, and then disease activity index (DAI) was evaluated and calculated. Pathological changes in the colon were observed by HE staining. The levels of anti-flagellin antibody, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in the serum were measured by ELISA. The expression levels of Toll-like receptor 5 (TLR5), myeloid differentiation factor 88 (MyD88) and nuclear factor kappa-Bp65 (NF-κBp65) in the colon tissues were evaluated by Western blot analysis and the activation of lymphocytes in mesenteric lymph node (MLN) was detected by flow cytometry. Results Compared with the control group, DAI scores in the model group were significantly raised, the colon length was significantly shortened, and the epithelium and intestinal gland disappeared. In addition, the serum levels of anti-flagellin antibody, IL-6, TNF-α and the protein levels of TLR5, MyD88, NF-κBp65 in the colon significantly increased, and the activation of T lymphocytes in MLN went up in the model group. All symptoms above were alleviated in the mesalazine and paeoniflorin groups compared with the model group. Conclusion Paeoniflorin can attenuate UC in mice by inhibiting the expression of flagellin and TLR5, and the activation of T cells. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Colitis, Ulcerative; Colon; Dextran Sulfate; Glucosides; Lymphocyte Activation; Male; Mice; Mice, Inbred C57BL; Monoterpenes; Random Allocation; T-Lymphocytes; Toll-Like Receptor 5 | 2020 |
Protective effects of paeoniflorin on TNBS-induced ulcerative colitis through inhibiting NF-kappaB pathway and apoptosis in mice.
Paeoniflorin is traditionally used to treat inflammatory disorders. In our laboratory, we have scientifically validated the anti-inflammatory effect of paeoniflorin. In this study, it has been aimed to evaluate in vivo anti-inflammatory effect of paeoniflorin isolated from the dried peeled root of Paeonia lactiflora Pall. It was further intended to find out the probable mechanism of anti-inflammatory effect of paeoniflorin. The anti-inflammatory effect of paeoniflorin (15, 30 and 45mg/kg) was measured employing TNBS-induced ulcerative colitis model of acute inflammation. The TNBS injection resulted significant colitis formation when compared with un-injected mice. The anti-inflammatory effects of paeoniflorin for ulcerative colitis were assessed by body weight, colonic weight and length, macroscopic scores, and histopathological examinations. In addition, the colonic tissue levels of inflammation markers, including myeloperoxidase (MPO), IL-2, IL-6, IL-10, IL-12, IL-1β, TNF-α and IFN-γ were also determined to assess the effect of paeoniflorin. In addition, western blot demonstrated that paeoniflorin inhibited NF-kappaB signaling pathway and apoptosis in TNBS-induced ulcerative colitis tissues. In conclusion, all the findings of this study suggested that paeoniflorin has the anti-inflammatory effect in ulcerative colitis via inhibiting MAPK/NF-kappaB pathway and apoptosis in mice. Topics: Animals; Anti-Inflammatory Agents; Apoptosis; Colitis, Ulcerative; Colon; Cytokines; Extracellular Signal-Regulated MAP Kinases; Glucosides; Humans; Inflammation; Male; Mice; Mice, Inbred BALB C; Monoterpenes; NF-kappa B; Paeonia; Signal Transduction; Trinitrobenzenesulfonic Acid | 2017 |