RGD Reference Report - Total Glucosides of Peony Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid/Ethanol-Induced Colitis in Rats Through Adjustment of Th1/Th2 Cytokines Polarization. - Rat Genome Database
Total Glucosides of Peony Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid/Ethanol-Induced Colitis in Rats Through Adjustment of Th1/Th2 Cytokines Polarization.
Authors:
Zhang, Y Zhou, R Zhou, F Cheng, H Xia, B
Citation:
Zhang Y, etal., Cell Biochem Biophys. 2013 Jun 15.
The present study is to investigate effects of total glucosides of peony (TGP) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced colitis in rats and to explore potential clinical use of TGP for treatment of inflammatory bowel disease. Sixty Sprague-Dawley rats were randomly grouped into normal controls, model controls, sulfasalazine (SASP) controls (100 mg/kg/day), and low, medium, and high-dose TGP groups (25, 50, and 100 mg/kg/day, respectively). 24 h following colonic instillation of TNBS, TGP, and SASP were given by gastric gavage three times a day for 7 days. Disease activity index (DAI), colon macroscopic damage index (CMDI), histopathological score (HPS), and myeloperoxidase (MPO) activity were evaluated. Levels of serum TNF-alpha, IL-1beta, and IL-10 were measured by ELISA, and expression of TNF-alpha, IL-1beta, and IL-10 mRNA and protein in colonic tissues was detected by RT-PCR and western blot, respectively. Compared with rats in the model controls, TGP (50 or 100 mg/kg/day)-treated rats with TNBS/ethanol-induced colitis showed significant improvements of DAI, CMDI, HPS, and MPO activity. Moreover, administration of TGP (50 or 100 mg/kg/day) decreased the up-regulated levels of serum TNF-alpha and IL-1beta, and expression of TNF-alpha and IL-1beta mRNA and protein in colonic tissues, and increased the serum IL-10 and colonic IL-10 mRNA and protein level. And there was no significant difference compared with administration of SASP (P > 0.05). TGP attenuates TNBS/ethanol-induced colitis in rats and its efficacy is similar to SASP, the potential mechanism might be related to the adjustment of Th1/Th2 cytokines polarization by decreasing pro-inflammatory cytokine TNF-alpha and IL-1beta, and increasing anti-inflammatory cytokine IL-10.