The Regulation Of PYY On TNBS-induced IBD Model Mouse And Associated Cytokines

Inflammatory Bowel Disease(IBD), a chronic nonspecific disease,includesulcerative colitis(UC) and Crohn`s disease(CD), with different histologic cytokineproperties.The exact pathogenesis of IBD is not fully clear. The interaction ofgenetic,immune, environment and infection contribute to IBD, and the abnormalimmune response and adjustment is the core to the IBD pathogenesis.Peptide YY(PYY) is peptide with amidation carboxyl terminal, and is straightchain composed of36amino acid polypeptide, amino and carboxyl terminal acidresidues are Tyrosine. PYY, in the forms of PYY1-36and PYY3-36, exists in thecirculatory system. The main physiological function of PYY is involving in theregulation of gastrointestinal function, such as inhibiting gastric emptying and gastricacid secretion, duodenum and jejunum movement,jejunum and colon mucosasecretion, gallbladder emptying and pancreatic exocrine and insulin secretion,stimulating the intestinal epithelial hyperplasia. Some researches showed that PYYhad inhibition of inflammation and can promote the improvement of pancreatitis.Some studies have showed that PYY, compared with normal people, concen-tration changed in plasma of patients with IBD, prompting PYY may be associatedwith IBD. Trinitrobenzene sulfonic acid induces IBD mice model, semi-quantitativePCR detects PYY and its receptors expression change of IBD model mice. Detedtingthe effect of PYY on pathological damage and inflammatory response by histologicgrading, MPO and ELISA after intraperitoneal injection of PYY to IBD model mouse.Isolating and culturing mouse peritoneal macrophages, semi-quantitatve PCR andELISA for detecting PYY on macrophages secreting the TNF-alpha,IL-6in vivo andin vitro. Testing the influence of PYY on spleen lymphocyte differentiation by flowcytometry in vivo and in vitro,to clear the effect of PYY on IBD, and reveal themechanism of immune regulation.The experimental results showed that PYY receptors expression changedsignificantly, clinical and pathological symptoms of IBD obviously reduced afterintraperitoneal injection of PYY. The secretion of TNF-alpha,IL-6decreased remarkblely, and the T lymphocyte differentiation was also affected. In vitro studiesreveal that PYY regulates and obviously inhibits LPS-induced macrophages secretingTNF-alpha,IL-6. Compared with PYY1-36, PYY3-36has more prominent inhibitionon LPS-induced macrophage secretion of IL-6. In addition, PYY regulates Th1/Th2differentiation. This study shows that PYY can adjust natural immune and acquiredimmune response in IBD by inhibiting secretion of macrophage inflammatorycytokines, improving the Th1/Th2differentiation imbalances, thereby inhibiting thethe IBD inflammation.This article reveals the function of PYY in IBD, and issue the mechanism fromimmune response, which will provide theoretical basis and a new train of thought forthe prevetion and treatment on IBD.