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Background: Inflammatory bowel disease (inflammatory bowel disease, IBD) is a group of long-term recurrent episodes of abdominal pain, diarrhea, mucous pus manifestations of inflammatory bowel disease, including ulcerative colitis (ulcerative colitis, UC) and Crow En disease (Crohn's disease, CD), having the characteristics of chronic and expendable. The incidence and prevalence of the disease in the world are reported to have continued to increase. The the of IBD etiology and pathogenesis is still unclear, one of the reasons leading to the pathogenesis of IBD immune disorders, subsets of Th17 cells and regulatory T cells disorders is one of the important part. At this stage, the treatment of IBD is very limited, mainly 5 - amino salicylic acid preparations, glucocorticoids, immunosuppressants, and recently used biological agents, but these drugs are there different limitations and side effects. Therefore, seek new and effective drugs has been a hot spot in the IBD Research. The TGP (total glucosides of paeony, TGP) is the active ingredient extracted from the traditional Chinese medicine white peony, the paeoniflorin (Paeoniflorin PF). Studies have shown, TGP has a certain function of immune regulation, inhibition of inflammation, but its role in the treatment of IBD are not yet clear. Objective: ① observed TNBS-induced changes in rats with experimental colitis, IL-6, IL-17, IL-23, and TGF-β1 in of Foxp3 experimental indicators, analysis of the relationship between these indicators and the incidence of experimental colitis. ② The the TGP on rats with experimental colitis induced by TNBS intervention to explore whether the anti-inflammatory effects on experimental colitis. ③ observed TGP on TNBS experimental colitis in rats induced by IL-6, IL-17, IL-23, and TGF-β1 in of Foxp3 experimental indicators. The ④ analysis TGP on the relationship between the intervention effect of experimental colitis and related experimental indicators discussed TGP possible pharmacological mechanism of action in experimental colitis. Methods: 60 SPF (Specific pathogen Free Specific Pathogen Free) SD rats were randomly divided into colitis model group and normal control group (0.9% NaC1 solution enema), the TGP high dose group (100 mg / kg), the TGP middle dose group (50mg/kg), the TGP the low-dose group (25mg/kg) and 5-ASA drugs control group (100 mg / kg), trinitrobenzene sulfonic acid (TNBS) / ethanol solution enema induced colitis model. After successful modeling, drug intervention group given the the TGP or 5-ASA orally, colitis model group and normal control group to be 0.9% NaC1 solution orally, intragastrically 14 days, the daily line disease activity index (DAI), 14d after anatomical lesion on the colon the index (CMDI) and histological damage index (TDI) score, the ELISA serum IL-6, IL-17 and IL-23 levels, SP immunohistochemical assay colon tissue TGF-β1 of Foxp3 expression. Results: colitis model group and normal control group CMDI TDI, of DAI mean significantly lower (0.90 ± 0.74vs6.88 ± 0.84,0.70 ± 0.48vs5.63 ± 0.48,0.11 ± 0.05vs1.41 ± 0.21, P lt; 0.05), serum IL-6, IL-17 and IL-23 content was significantly lower (62.12 ± 16.034vs350.21 ± 79.80,188.04 ± 72.71vs 547.38 ± 270.67,11.80 ± 1.82vs 44.13 ± 30.08, all P lt; 0.05), the colon tissue TGF-β1 and Foxp3 content was significantly higher (190.15 ± 51.79vs 69.45 ± 11.15,206.21 ± 76.09vs116.08 ± 21.02, P lt; 0.05). 5-ASA in high doses TGP can significantly reduce the DAI mean CMDI and TDI (0.96 ± 0.15,1.18 ± 0.21,0.92 ± 0.20 vs1.41 ± 0.21; 2.78 ± 2.11,3.78 ± 1.86,3.56 ± 1.94 vs 6.88 ± 0.84; 2.22 ± 0.83,3.56 ± 1.51,2.44 ± 1.51 vs 5.63 ± 0.74, all P lt; 0.05), lower serum IL-6, IL-17 and IL-23 content (156.53 ± 52.06,210.54 ± 106.58,168.77 ± 63.91 vs 350.21 ± 79.80; 317.41 ± 80.91,317.40 ± 76.67,244.76 ± 126.58 vs 547.38 ± 270.67; 17.17 ± 4.26,18.55 ± 5.76,14.51 ± 1.69 vs 44.13 ± 30.08, all P lt; 0.05) elevated colonic tissue TGF-β1 and Foxp3 content (177.72 ± 37.28,131.46 ± 62.87,154.59 ± 49.55 vs 69.45 ± 11.15; 244.84 ± 118.45,184.38 ± 84.56, 201.74 ± 86.09 vs 116.08 ± 21.02, P lt; 0.05). ② colitis model colon tissue TGF-β1, Foxp3 was negatively correlated with serum IL-6, IL-17 and IL-23 (r = -0.936, r = -0.985, r = -0.944 and r = -0.871, r = -0.944, r = -0.852, all P lt; 0.05); the white peony the total glycosides high dose treatment group colon tissue TGF-β1, Foxp3 negatively correlated with serum IL-6, IL-17 and IL-23 was ( r = -0.839, r = -0.869, r = -0.835 and r = -0.870, r = -0.884, r = -0.911, all P lt; 0.05); TGF-β1 in colonic tissue of 5-ASA treatment group of Foxp3 and serum IL-6, IL-17 and IL-23 showed a negative correlation (r = -0.854, r = -0.724, r = -0.954 and r = -0.931, r = -0.873, r = -0.740, both P lt ; 0.05). Colitis model group colon tissue TGF-β1, Foxp3 rats DAI, CMDI, TDI score was negatively correlated (r = -0.928, r = -0.950, r = -0.883 and r = -0.925, r = -0.905, r = -0.774, all P lt; 0.05); white peony root the total glycosides high dose group colon tissue of TGF-β1, Foxp3 and rats DAI, CMDI, TDI score showed a negative correlation (r = -0.685, r = -0.728, r = -0.765 and r = -0.765, r = -0.765, r = -0.737, P lt; 0.05); 5-ASA treatment group colon tissue TGF-β1, Foxp3 rats DAI, CMDI, TDI score was negative correlation (r = -0.926, r = -0.894, r = -0.934 and r = -0.811, r = -0.860, r = -0.824, all P lt; 0.05). Model group, serum IL-6, IL-17, IL-23 and rat DAI, CMDI, TDI score showed a positive correlation (r = 0.874, r = 0.930, r = 0.885; r = 0.919, r = 0.947, r = 0.928 ; r = 0.766, r = 0.890, r = 0.794, P lt; 0.05); of the white peony the total glycosides high dose levels of serum IL-6, IL-17, IL-23 and rat DAI, CMDI, TDI score was being related (r = 0.746, r = 0.954, r = 0.929; r = 0.730, r = 0.911, r = 0.894; r = 0.811, r = 0.762, r = 0.719, both P lt; 0.05); 5-ASA therapy serum levels of IL-6, IL-17, IL-23 and rat DAI, CMDI, TDI score was positively correlated (r = 0.873, r = 0.944, r = 0.873; r = 0.787, r = 0.929, r = 0.896; r = 0.843, r = 0.756, r = 0.860, all P lt; 0.05). Was no statistically significant difference between ③ high-dose group and the 5-ASA group TGP above indicators. Conclusion: TNBS-induced colitis in rat serum IL-6, IL-17 and IL-23 expression increased and was positively correlated with the degree of inflammation; colitis colon tissue expression of TGF-β1 and Foxp3. and negatively correlated with the degree of inflammation was. TGP, and 5ASA able to significantly reduce the serum levels of IL-6, IL-17 and IL-23 reduction, increased colitis colon tissue TGF-β1 and Foxp3 expression. TGP may by up-regulating TGF-β1 and Foxp3 level, to promote the expression of CD4 CD25 Treg cells, reduced IL-6, IL-23 expression, thereby inhibiting the activation of Th17 cell populations, reducing IL-17 and IL-6 expression, which alleviate the symptoms of rats with experimental colitis induced by TNBS colitis injury.
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