Published online Jul 14, 2026. doi: 10.3748/wjg.v32.i26.118923
Revised: February 26, 2026
Accepted: March 17, 2026
Published online: July 14, 2026
Processing time: 162 Days and 16.3 Hours
Chronic radiation proctitis (CRP), a major complication of pelvic radiotherapy, lacks effective treatments and a standardized animal model that recapitulates its late fibrotic and angiogenic pathologies.
To establish a model that recapitulates the features of human CRP and to inve
Rats were randomized into a control group and single-dose irradiation groups (12.5-37.5 Gy). Rectal injury was assessed via 6-month continuous endoscopic observation, the modified Vienna Rectoscopy Score, and histological analysis. Additionally, rectal tissues were analyzed for cytoskeletal protein alterations.
Acute mucosal injury was reversible at doses below 20 Gy. In the 20-35 Gy groups, persistent radiation proctitis, marked telangiectasia, and severe mucosal fibrosis indicated irreversible injury. Furthermore, cytoskeletal proteins, particularly tubulin, decreased sharply at doses ≥ 20 Gy. Vascular endothelial growth factor was mildly upregula
Single-dose radiation (20-35 Gy) induces CRP. Reduced tubulin expression marks the early transition to chronic injury (P < 0.0001).
Core Tip: Chronic radiation proctitis can be induced by a single dose of 20-35 Gy irradiation, which simplifies the modeling procedure while recapitulating two major human pathological features: Telangiectasia and progressive fibrosis. The formation of chronic injury is associated with the destruction of microtubule protein, the low expression of tubulin at 2 weeks after irradiation can serve as an early indicator for the transition of rectal toward chronic radiation injury. After radiation without intervention, around the eighth week, chronic manifestations such as capillary dilation would appear. The observation period for the therapeutic effect should be extended to at least 8 weeks.