Chinese Journal of Tissue Engineering Research ›› 2020, Vol. 24 ›› Issue (29): 4673-4679.doi: 10.3969/j.issn.2095-4344.2817

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Protective effect of crocin in ulcerative colitis rats and its related mechanism

Yang Minjie1, Liu Wei2, Tu Hongfei2, Li Li2, Fei Sujuan2   

  1. 1Gastroenterology Research Center, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu Province, China; 2Department of Gastroenterology, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu Province, China
  • Received:2020-02-12 Revised:2020-02-22 Accepted:2020-03-18 Online:2020-10-18 Published:2020-09-14
  • Contact: Fei Sujuan, Master, Chief physician, Master’s supervisor, Department of Gastroenterology, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu Province, China
  • About author:Yang Minjie, Master candidate, Gastroenterology Research Center, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu Province, China
  • Supported by:
    the Scientific Research Program of the Jiangsu Provincial Health and Family Planning Commission, No. H2017082; Xuzhou Science and Technology Key Research & Development Plan Project, No. KC17184

Abstract:

BACKGROUND: Crocin has anti-inflammatory and anti-oxidative stress effects. The therapeutic effects of crocin on ulcerative colitis and related mechanisms are still unclear.

OBJECTIVE: To explore the protective effect of crocin in ulcerative colitis rats and its related mechanism.

METHODS: Thirty Sprague-Dawley rats were randomly divided into five groups: normal group, model group, low-dose crocin group, high-dose crocin group, and positive control group. Experimental rat model of ulcerative colitis was induced by dextran sodium sulfate. Starting on the first day of modeling, rats were routinely fed in the normal group, were given sulfasalazine by gavage in the positive drug group, and were gavaged with 0.05 and 0.1 g/kg crocin in the low- and high-dose crocin groups, respectively.

RESULTS AND CONCLUSION: One week after intervention, the crocin-treated rats had significantly decreased scores on colon tissue injury and Crohn’s disease activity index (P < 0.05). Compared with the model group, crocin groups had a decrease in the content of malondialdehyde and activity of myeloperoxidase (P < 0.05), and an increase in the activity of superoxide dismutase in the colon tissue (P < 0.05). Shown by immunohistochemical staining, compared with the model group, treatment with crocin significantly reduced immune responses of tumor necrosis factor α and interleukin 23 proteins after 1 week of intervention (P < 0.05). Compared with the model group, treatment with crocin downregulated the expression levels of total protein Bax, Caspase-3, Toll-like receptor 4 and MyD88 (P < 0.05), and upregulated the expression of Bcl-2 in the intestinal tissue of rats (P < 0.05). These results indicate that crocin has a certain therapeutic effect in ulcerative colitis rats and its mechanism may be related to down-regulation of the Toll-like receptor 4/MyD88 signaling pathway and inhibition of oxidative stress, inflammation and apoptosis in the colon.

Key words: crocin, dextran sulphate sodium, ulcerative colitis, animal model, Toll-like receptor 4/MyD88, tumor necrosis factor-α, interleukin23, oxidative stress, apoptosis, rat

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