Protective Effect of Erqi Decoction on Intestinal Tract of Acute Radiation Intestinal Injury Rats and Its Mechanism / 广州中医药大学学报

ABSTRACT

Objective To investigate the protective effects of Erqi Decoction(EQD; mainly composed of Radix Aristolochiae Kaempferi, Radix Rhizoma Seu Flos Cypripedii, Cortex Fraxini, Cortex Phellodendri, Radix et Rhizoma Rhei) on the intestinal tract in rats with acute radiation intestinal injury and its mechanism. Methods Sixty SD rats were randomly divided into normal group, model group, EQD group and Baitouweng Decoction group (BD group), 15 rats in each group. The acute radiation enteritis model was established by exposing the whole abdomen to a total dose of 10 Gy of 6 MV higher-energy X-rays. EQD group and BD group were given intragastrical administration with corresponding medicine of EQD at the dose of 8.85 g·kg-1·d-1, BD at the dose of 4.69 g·kg-1·d-1 respectively, and the normal group and the model group were given intragastrical administration with the same volume of normal saline. The treatment lasted for 7 continuous days. After modeling, the morphological change of the proximal ileum tissue was observed under light microscope. Villus height, crypt depth, and thickness of the ileal mucosa and entire wall were measured by image analysis system. The myeloperoxidase (MPO) content in ileum tissue was determined by spectrophotometer, and the expression levels of caspase -3 and proliferating cell nuclear antigen (PCNA) in ileum tissue were determined by immunohistochemistry. Results EQD group and BD group had milder injuries of the ileal structure, and had higher villus height, crypt depth, and thickness of mucosa and entire wall than those in the model group (P 0.05). MPO content in EQD group and BD group was decreased(P0.05). Conclusion EQD has certain protective effects against radiation-induced intestinal damage, which mechanism is probably associated with relieving the local intestinal inflammatory reaction, accelerating intestinal epithelial cell proliferation, and inhibiting intestinal epithelial cell apoptosis.