Objective To explore the possible mechanism of Shenshuai Formula Ⅱ（肾衰Ⅱ号） in treating chronic kidney failure（CKF）. Methods CKF rats model was established by 5/6 nephrectomy in SD rats. Thirty successfully modeled rats were randomly divided into a model group

a Shenshuai Formula Ⅱ group

and bifid triple viable group

with 10 rats in each group; a blank group of 10 rats was also set. Concentration of 6.09 g/ml Shenshuai Formula Ⅱ at dose of 10 ml/kg and concentration of 17.86 mg/（kg·d） bifid triple viable were given by gavage to the rats in the corresponding groups; 2 ml normal saline was given by gavage to the rats in the blank group and model group; all interventions were performed once daily for 60 days. The rats were fasted for five hours before being fed with 10 mg/kg endotoxin（LPS）; after 3.5 hours

the rats were anesthetized in the abdominal cavity to collect and separate serum

and the small intestine was fixed with 10% formalin. The serum creatinine

urea nitrogen and LPS content were assessed. HE staining method was used to observe the pathological structure of intestinal tissue. The intestinal tissue atresia protein（Occludin）

zonula atresia protein 1（ZO-1）

myosin light chain kinase（MLCK）

muscle globulin light chain（MLC） protein and the mRNA expression

and phosphorylated myosin light chain（p-MLC） protein expression were detected. Results Compared to the blank group

the model group had higher levels of serum creatinine

urea nitrogen and LPS content

higher expression of MLCK

p-MLC protein and MLCK mRNA

and lower expression of ZO-1 and Occludin protein and mRNA（P<0.05）; and the pathological results showed that small intestinal villi became shorter and wider; local crypts elongated; and gland proliferation was not active. Compared to the model group

Shenshuai Formula Ⅱ group had lower serum creatinine

urea nitrogen and LPS content

lower expression of MLCK protein and mRNA and p-MLC protein

and higher expression of ZO-1 and Occludin protein（P<0.05）; and the intestinal pathological results were improved. Conclusion Shenshuai Formula Ⅱ may reduce the transcription and expression of MLCK in the intestinal tissue

reduce the phosphorylation level of MLC

and repair the tight junction structure

thereby adjusting the intestinal barrier function and reducing the entry of intestinal endotoxin into the blood so as to treat CKF.