Objective:To investigate the curative effect and the mechanism of Xinmaixian powder in ulcerative colitis(UC) rats by observing its regulatory effect on protein kinase R like endoplasmic reticulum kinase (PERK)/eukaryotic translation initiation factor-2α(eIF-2α)/nuclear factor-κB(NF-κB) signaling pathway. Method:Sixty SD rats were randomly divided into six groups:normal group

model group

mesalazine group

Xinmaixian powder low

middle and high dose groups

with 10 rats in each group.After UC models were successfully prepared by dextran sodium sulfate(DSS)

the rats in mesalazine group received mesalazine sustained-release granules suspension in the dose of 0.42 g·kg-1·d-1 for 14 days; the rats in Xinmaixian powder low

middle and high dose groups were treated with Xinmaixian powder suspension in the dose of 1.5

3

and 6 g·kg-1·d-1 respectively for 14 days.The other groups were treated with same volume of normal saline for 14 days.Finally

the scores of disease activity index (DAI) were evaluated; and expression levels of NF-κB in serum were tested by enzyme-linked immunosorbent assay(ELISA).In addition

protein expression levels of PERK and eIF-2α in colonic tissues were detected by Western blot

while mRNA expression levels of PERK and eIF-2α in colonic tissues were detected by Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR). Result:DA-I scores

expression levels of NF-κB in serum and the protein and mRNA expression levels of PERK and eIF-2α in colonic tissues in the model group were significantly higher than those in normal group(P<0.05). As compared with the model group

Xinmaixian powder groups can reduce DAI scores and expression levels of NF-κB in serum(P<0.05)

and the protein and mRNA expression levels of PERK and eIF-2α were also decreased in Xinmaixian powder middle and high dose groups(P<0.05). Conclusion:Xinmaixian powder has a good curative effect on UC rats

and its therapeutic mechanism may be related to inhibiting the activation of PERK/eIF-2α/NF-κB signaling pathway.