黄芪多糖对梗阻性黄疸大鼠肠损害的治疗作用及其机制探讨.

Objective To observe the effect of Astragalus polysaccharide ( APS) on intestinal damage in obstructive jaundice (OJ) rats and to explore its possible mechanism. Methods Forty-eight Wistar rats were randomly divided into the intervention group, model group, and control group, with 16 rats in each. The OJ models were prepared in the intervention group and model group, and in the control group, only the common bile ducts of rats were isolated. At 24 h after modeling, the rats in the intervention group were orally administered APS normal saline solution ( 100 mglkg), and the control group and the model group with the same amount of normal saline, twice a day. Blood was taken from rats in each group at 14 days after modeling, and the serum diamine oxidase ( DAO) and intestinal fatty acid binding protein ( I-FABP) were detected by ELISA. After the blood was taken, the rats were sacrificed, and the small intestine tissues were taken. The proliferating cell nuclear antigen ( PCNA) protein was detected by Western blotting. The depth of glandular fossa and the height of villi were observed under an optical microscope. The terminal deoxynucleotidyl transferase dUTP nickel terminallabeling method (TUNEL) was used to count the number of apoptotic cells. IL-1β, IL-lRa, IL-10, TLR4 and NF-KB P65 positive cells were detected by immunofluorescence staining, and TLR4 and NF-KB P65 proteins were detected by Western blotting. Results Significant pathological damage occurred in the small intestine of rats in the model group. The levels of serum DAO, I-FABP, and TNF-α and IL-1β expression in the tissues were higher, while the tissue IL-l Ra, IL-10 levels were lower in the model group than in the control group (all P<0.05). The pathological damage of small intestine tissues became less in the intervention group; the levels of serum DAO, I-FABP, and TNF-α and IL-lβ expression in the tissues were lower, but the levels of IL-l Ra and IL-10 in the tissues were higher in the intervention group than in the model group (all P<0.05). Conclusions APS has a therapeutic effect on intestinal damage in OJ rats. It can protect the intestinal mucosal barrier of rats and resist small intestinal epithelial cell apoptosis by maintaining the anti-inflammatory and pro-inflammatory balance through the TLR4/NF -KB P65 pathway. [ABSTRACT FROM AUTHOR]