Objective

2

To explore the mechanism of Sishenwan， Baitouweng Tang， and Lianlitang in the treatment of ulcerative colitis （UC）， and compare their efficacies on UC in rats.

Method

2

Ninety SD rats of SPF grade were randomly divided into blank group （distilled water， 2 mL·d

-1

） and experimental group. The rats in the experimental groups were administered with 2，4，6-trinitrobenzene sulfonic acid （TNBS） by clysis to induce the UC model. Subsequently， the model rats were divided into a model group （distilled water， 2 mL·d

-1

）， positive group ［sulfasalazine （SASP）， 0.4 g·kg

-1

·d

-1

］， Sishenwan group （1.76 g·kg

-1

·d

-1

）， a Baitouweng Tang group （1.40 g·kg

-1

·d

-1

）， and Lianlitang group （2.13 g·kg

-1

·d

-1

） according to the random number table. The rats in each group were dosed at 2 mL·d

-1

for 14 days. The pathological score for colonic mucosa was detected. Cytokines were detected by the cytokine chip. The enzyme-linked immunosorbent assay （ELISA） was used to detect the free triiodothyronine （FT

3

）， glucagon-like peptide-1 （GLP-1）， and corticosterone （CORT） in plasma， and neurotensin （NT）， substance P （SP）， vasoactive intestinal peptide （VIP）， and somatostatin （SST） in colon tissues.

Result

2

Compared with the normal group， the model group showed increased colon mass-length ratio and pathological score for colonic mucosa （

P

<

0.01）， infiltration of massive lymphocytes， disordered or absent intestinal villi， elevated levels of cytokine-induced neutrophil chemoattractant-1/2

α

/

β

/3 （CINC-1/2

α

/

β

/3）， interleukin-1

α

（IL-1

α

）， interferon-inducible protein-10 （IP-10） and other factors in colon tissues （

P

<

0.05）， dwindled CORT and GLP-1 levels in plasma （

P

<

0.05）， and increased SP content in colon tissues （

P

<

0.05）. Compared with the results in the model group， the mucosal injury in the colon of rats in each drug group was relieved. The levels of IL-1

α

， IP-10， lipopolysaccharide-inducible CXC chemokine （LIX）， and L-selectin of rats in the Lianlitang group and Sishenwan group were reduced （

P

<

0.05）， and the CINC-3 and IL-17 levels were diminished in the Baitouweng Tang group （

P

<

0.05）. The levels of CINC-1/3， IL-1

α

， and IP-10 were reduced in the SASP group （

P

<

0.05）. The plasma FT

3

was up-regulated in the Lianlitang group， and the plasma GLP-1 levels were elevated in the three Chinese medicine groups （

P

<

0.05）. The VIP content in colon tissues of the Sishenwan group and Baitouweng Tang group was down-regulated （

P

<

0.05）， and the SST content in colon tissues of the SASP group was significantly up-regulated （

P

<

0.01）.

Conclusion

2

The intervention of Lianlitang and Sishenwan on UC was significant， and the underlying mechanism of action might be related to inflammation inhibition and immune balance by regulating the cytokine network. The efficacy of Lianlitang was predominant， followed by Sishenwan and Baitouweng Tang.