Published online Apr 7, 2022. doi: 10.3748/wjg.v28.i13.1315
Peer-review started: September 20, 2021
First decision: January 9, 2022
Revised: January 17, 2022
Accepted: February 27, 2022
Article in press: February 27, 2022
Published online: April 7, 2022
Processing time: 191 Days and 9 Hours
In recent years, increasing attention has been paid to the study of osteopenia and osteoporosis caused by inflammatory bowel disease (IBD). Osteoporosis is one of the more common extra-intestinal manifestations in IBD patients. No effective preventive or treatment modality exists for osteoporosis in IBD patients. Therefore, we explored the possible pathogenesis of IBD-induced osteoporosis and evaluated the effectiveness of a promising drug in the present study.
Jianpi Qingchang Bushen decoction (JQBD) is a prescription developed by our team to treat IBD patients with osteoporosis. In this study, the potential pharmacodynamic mechanism of JQBD for treating IBD-induced osteoporosis was studied in vivo.
The effects of JQBD on the inflammatory response and bone metabolism were observed to provide a theoretical basis for the clinical prevention and treatment of osteoporosis in IBD patients.
An IBD-induced osteoporosis model was constructed by treating interleukin-10-knockout mice with piroxicam. JQBD was given as an intervention, and its effect on the inflammatory response and bone metabolism was observed.
Our data show that JQBD was protective against IBD-induced bone loss by inhibiting inflammation. The receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL), osteoprotegerin (OPG), receptor activator of NF-κB (RANK), and NF-κB protein levels increased significantly in colon tissue from the model group. Their expression levels were downregulated after JQBD intervention.
We evaluated the curative effects of JQBD on the bone-loss IBD model mice and confirmed that the RANK/RANKL/OPG signaling pathway is involved in the process.
This study primarily focused on the mechanism by which JQBD regulates the RANK/RANKL/OPG signaling pathway and improves IBD-induced osteoporosis.