期刊
JOURNAL OF ETHNOPHARMACOLOGY
卷 269, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113716
关键词
Jiaolong capsule; Colitis; Toll like receptor 4
资金
- National Natural Science Foundation of China [81302787]
- Postdoctoral Science Foundation of China [2018M633405]
- Shaanxi Province Natural Science Foundation [2019JQ-562]
- Shaanxi Administration of Traditional Chinese Medicine [2019-ZZ-JC014]
The study demonstrated that Jiaolong capsule (JLC) has a beneficial effect on treating colitis in a rat model by restoring colonic structure, repairing damage, rebalancing intestinal microbiota, and suppressing inflammation pathways.
Ethnopharmacological relevance: Jiaolong capsule (JLC) was approved for the therapy of gastrointestinal diseases by the State Food and Drug Administration (SFDA) of China. It has a satisfactory curative effect in the treatment of patients with inflammatory bowel disease, however, the mechanism remains to be elucidated. Aim of the study: In current study, the effects and possible mechanisms of JLC on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated. Materials and methods: Sulfasalazine and JLC were administrated orally and initialized 6 h after TNBS enema, once a day for seven consecutive days. The effect of JLC on intestinal microbial populations and LPS/TLR-4/NF-kappa B pathway was observed and assessed. Thirty female SD rats were distributed into six groups randomly and equally, namely, control, TNBS, TNBS + sulfasalazine (625 mg/kg), and TNBS + three different doses of JLC (25, 50, and 100 mg/kg) groups. Results: The effect of JLC on restoring normal structures of colorectum and repairing colonic damage were superior to that of sulfasalazine. JLC showed a positive effect in re-balancing intestinal bacteria population of colitis, and suppressed the activation of LPS/TLR-4/NF-kappa B pathway. Conclusion: The results suggest that JLC demonstrated a beneficial effect on treating colitis in a rat model. The possible mechanisms may be through the regulatory effect of intestinal commensal bacteria and down-regulation of LPS/TLR-4/NF-kappa B pathway.
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