Objective To explore the possible mechanism of Chaishao Liujun Decoction（CSLJD

柴芍六君汤） in the treatment of chronic atrophic gastritis（CAG） with liver constraint and spleen deficiency pattern. Methods Forty-two SD rats were randomly divided into blank group（10 rats） and modeling group（32 rats）. In model group

the rat model of CAG with liver constraint and spleen deficiency pattern was replicated by the compound factor modeling method. Thirty successful modelling rats were randomized into model group

vitacoenzyme group and CSLJD group

with 10 rats in each group. The CSLJD group was gavaged with 10 ml/（kg·d） of 0.51 g/ml CSLJD; vitacoenzyme group was gavaged with 10 ml/（kg·d） of 24 mg/ml vitacoenzyme suspension; blank group and model group were gavaged with the same volume of sterilized drinking water; all the interventions lasted for 4 weeks. The body mass and pathological changes of gastric mucosa in rats were assessed. The mRNA expression of nuclear transcription factor-κB（NF-κB） and proto-oncogene（c-Myc） and protein expression of transcription-activated protein 1（STAT1） were detected. Results There was no statistically significant difference in the body mass increase of rats between groups（P>0.05）. The glands in lamina propria of gastric mucosal in the model group were atrophied

arranged sparsely and disorderly

lost of parietal cells and principal cells

and with more inflammatory infiltration; the expressions of NF-κB and c-Myc mRNA and STAT1 protein were significantly higher than those of the blank group（P<0.01）. Compared to those in the model group

the expression of NF-κB mRNA in CSLJD group and the expression of c-Myc mRNA in vitacoenzyme group decreased（P<0.05）; the pathological changes of gastric mucosa in both groups were improved with varying degrees; the inflammatory infiltration was alleviated; the expression of STAT1 protein was inhibited（P<0.05 or P<0.01）. The expression of NF-κB mRNA in CSLJD group was lower than that in vitacoenzyme group（P<0.05）. Conclusion CSLJD can improve atrophic gastric mucosa and has therapeutic effect on CAG rats with liver constraint and spleen deficiency pattern. Its mechanism may be related to inhibiting the abnormal activation of NF-κB/STAT1 and down-regulating the overexpression of NF-κB mRNA and STAT1 protein in gastric mucosa.