Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Rhizoma atractylodis suppresses TNBs-induced colitis through NF-κB signaling pathway

Guanjun Wang¹, Yunxin Ji² , Ni Dai³, Yanbin Hou³

¹Department of Psychosomatic Medicine Ningbo First hospital 315010, China; ²Department of Ophthalmology Ningbo Huachi hospital 315010, Ningbo First hospital?No.59 Liuting Road, Ningbo China; ³Department of Psychosomatic Medicine Ningbo First hospital 315010, China.

For correspondence:- Yunxin Ji Email: ncv4589@126.com Tel:+8616579322981

Accepted: 23 August 2021 Published: 30 December 2021

Citation: Wang G, Ji Y, Dai N, Hou Y. Rhizoma atractylodis suppresses TNBs-induced colitis through NF-κB signaling pathway. Trop J Pharm Res 2021; 20(12):2503-2510 doi: 10.4314/tjpr.v20i12.7

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: Colitis is a kind of chronic non-specific inflammatory disease with increasing morbidity worldwide. Rhizoma atractylodis is the dry rhizome of Atractylodes lancea, which is often used to treat inflammations, but its connection with colitis is yet to be understood. Thus, the study was to confirm the functions of Rhizoma atractylodis on colitis cell progression.

Methods: Cells of human colonic epithelial cell line, NCM460 were induced by trinitrobenzene sulfonic acid (TNBs) to create inflammatory TNBs-NCM460 model groups, while untreated NCM460 cells were taken as normal control group. Varying concentrations (0, 20, 50 and 100 μmol/L) of Rhizoma atractylodis were added to pretreat the NCM460 cells before exposure to TNBs. RT-qPCR and Elisa methods detected the mRNA expression and protein concentrations of IL-6 and TNF-α and Western blot analyses were utilized to measure protein levels of NF-κB.

Results: Rhizoma atractylodis suppressed the Il-6 and TNF-α, which were induced by TNBs. Furthermore, the NF-κB pathway was inactivated in the cells with the pretreatment of hizoma atractylodis.

Conclusion: Rhizoma atractylodis inhibited inflammatory cytokines IL-6 and TNF-α through NF-κB inactivation. Therefore, rhizoma atractylodism might be a complementary medication in colitis.

Keywords: Cell progression, Colitis, NF-κB, Rhizoma atractylodis