RESUMEN
Objective:To investigate whether the therapeutic effect of Dahuang Mudan Tang on septic acute intestinal dysfunction in sepsis ratsis related to the regulation of expression of triggering receptor expressed on myeloid cells-1(TREM-1). Method:Totally 100 male SD rats were injected intraperitoneally with lipopolysaccharide (LPS) at a dose of 4.5 mg·kg-1 to build sepsis model. The sepsis model rats were randomly divided into five groups:model group, glutamine group (3.75 g·kg-1),low,medium, high-dose Dahuang Mudan Tang group(7.5,15,30 g·kg-1),and another 10 normal rats were selected as normal group. Seven days later,2 mL suspension (100 mg lactulose and 50 mg mannitol) was orally administrated by gavage, and 24 h urinewas collected. The ratio of lactulose to mannitol in urine (L/M) was detected by HPLC with pulsed electrochemical detection (HPLC-PED).Serum citrulline concentrationsin blood and ileum were determined by HPLC.Enzyme linked immunesorbent assay (ELISA) was used to detect the concentrations of triggering receptor expressed on myeloid cells-1(TREM-1),tumor necrosis factor-α(TNF-α),intestinal fatty acid binding protein(iFABP) and D-lactic acid.Real-time PCR was used to detect the mRNA expressions of TREM-1,Toll-like receptors2(TLR2),Toll-like receptors 4(TLR4),myeloid cell differentiation protein(MyD88),nuclear transcription factor-κB(NF-κB).Electron microscopy was used to observe the pathological changes of intestinal mucosa injury. Result:Compared with normal group, the serum concentrations of TREM-1,TNF-α,iFABP, D-lactate; the ratio of lactulose to mannitol in urine (L/M)and the expressions of TREM-1,TLR2,TLR4,MyD88,NF-κB mRNA in model group were increased obviously(PPPPPκB mRNA,and the serum concentrations of TREM-1 and TNF-α in all medication administration groups were decreased obviously(PD-lactate, L/M, the Chiu scorein glutamine group, medium-dose Dahuang Mudan Tang group and high-dose Dahuang Mudan Tang group were decreased obviously(PPPConclusion:Dahuang Mudan Tang can effectively treat SAID in rats, and its mechanism may be realized by regulating the expression of TREM-1 and relieving intestinal inflammation of intestinal tract.