The inhibitory effect of compound Q-l on proliferation of MH7A induced by TNF-α and its significance
10.3969/j.issn.1001-1978.2021.11.014
- Author:
Sha-Sha WU
1
;
Yan WANG
1
;
Ting XU
1
;
Xiao-Long LIU
1
;
Hai-Bing QIAN
1
Author Information
1. Guizhou University of Traditional Chinese Medicine, Guizhou Center for Consistency of Characteristic, Action and Utility of Genuine Regional Materia Medica
- Publication Type:Journal Article
- Keywords:
compound Q-l;
MAPK signaling pathway;
MH7A;
NF-KB signaling pathway;
rheumatoid ar-thritis;
TNF-α
- From:
Chinese Pharmacological Bulletin
2021;37(11):1554-1558
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of compound Q-L on MH7A based on NF-KB and MAPK signaling pathways and its mechanism. Methods Human rheumatoid arthritis fibroblast synovial cell line (MH7A) was selected as the experimental object. The effect of compound Q-l on the proliferation of MH7A cells was determined by CCK-8 method. The effect of compound Q-l on the migration ability of MH7A cells was detected by Transwell assay. TNF-α solution was used as inducer, and the content of TNF-α and IL-6 in cell supernatant was determined by ELISA. The protein expressions of p65, p-p65, IκBα, P-IκBα, p38, p-p38, ERK, p-ERK, JNK and p-JNK in the cells were determined by Western blot. Results Compound Q-l at different concentrations significantly inhibited the activity of MH7A cells. Compound Q-l significantly inhibited the migration of MH7A cells. Compound Q-l significantly reduced the contents of TNF-α and IL-6 in cell supernatant. Compound Q-l could significantly down-regulate the protein expression levels of p65, p-p65, P-IκBα, p38, p-p38 induced by TNF-α, but had no marked effects on IKBCX, ERK, p-ERK, JNK and p-JNK proteins. Conclusion Compound Q-l can significantly inhibit the proliferation of MH7A cells, reduce the expression of inflammatory cytokines TNF-α and IL-6 in cell supernatant, and down-regulate the protein expressions of p65, p-p65, IKBCX, p-LKBA, p38, p-p38 induced by TNF-α. The possible mechanism of action is related to NF-κB and p38MAPK sig-naling pathways.
