Published online May 7, 2019. doi: 10.3748/wjg.v25.i17.2071
Peer-review started: January 14, 2019
First decision: February 13, 2019
Revised: March 13, 2019
Accepted: March 15, 2019
Article in press: March 16, 2019
Published online: May 7, 2019
Processing time: 114 Days and 11.1 Hours
A20, as an intestinal epithelium protector, plays a critical role in anti-apoptosis in Crohn’s disease. Previous studies have indicated a beneficial role of herbs-partitioned moxibustion (HPM) in Crohn’s disease by decreasing intestinal epithelial apoptosis. However, whether the effect of HPM is through A20 is unclear.
Our findings will suggest a role of HPM in regulating A20 level in anti-apoptotic pathway in the intestinal epithelium of mice with Crohn’s disease.
To explore whether HPM alleviates cell apoptosis in the intestinal epithelium by upregulating A20 level in Crohn’s disease.
Two types of mice were included in this study, namely, mice with A20 deletion in intestinal epithelial cells (A20IEC-KO) and wild-type mice. Both of them were randomly divided into normal control (NC), model control (MC), mesalazine (MESA), and HPM groups. 2,4,6-trinitrobenzene sulfonic acid (TNBS) was administered to establish a Crohn’s disease model in the two types. The morphology of the colonic mucosa, serum endotoxin, apoptosis of epithelial cells, protein levels of A20 and tumor necrosis factor receptor (TNFR) 1-related signaling molecules, co-expression of A20 and TNFR1-associated death domain (TRADD), and co-expression of A20 and receptor-interacting protein (RIP) 1 were observed. All data are presented as the mean ± standard deviation.
Compared with A20IEC-KO mice, wild-type mice in the HPM group showed that damage of intestinal epithelial barrier was improved, serum endotoxin levels were significantly downregulated (P < 0.01), apoptosis percentages were significantly decreased (P < 0.01), A20 level was significantly upregulated (P < 0.01), and TNFR1, TRADDD, and RIP1 levels were downregulated (PTNF-a < 0.01, PTNFR1 < 0.05, PTRADD < 0.05, PRIP1 < 0.05). In addition, the co-expression of A20/TRADD and A20/RIP1 showed a predominant yellow fluorescence in WT HPM mice, while a predominantly red fluorescence was noted in A20IEC-KO HPM mice.
HPM can upregulate A20 level, resulting in decreased expression of TNFR1, TRADD, and RIP1 to alleviate aberrant cell apoptosis in the intestinal epithelial barrier in Crohn’s disease.
Effect of HPM in decreasing cell apoptosis of intestinal epithelial cells is through upregulating A20 level in Crohn’s disease.