Objective To explore the possible mechanism of Banxia Xiexin Decoction（BXD

半夏泻心汤） in the treatment of disorders of gastrointestinal motility（DGIM）. Methods Thirty SD rats were randomly divided into BXD group and deionized water group with 15 rats in each group. Correspondingly

BXD and deionized water at a dose of 12.15 g/（kg·d） were given by gavage for seven days

so as to prepare the BXD-contained and deionized water-contained serum. Gastric interstitial cells of Cajal（ICC） of rats were divided into blank group

deionized water group

and 5%

10% and 15% BXD group. The blank group was given 10% fetal calf serum

while the other groups were given either deionized water-contained or BXD-contained serum correspondingly; the dose was 2 mL in all the groups. The apoptosis of ICC was assessed

and the result was used to figure out the optimum concentration of BXD for conducting a further test

which include the blank group

the deionized water group and BXD group. In this further test

the drug concentration was same as mentioned above except for the BXD group which used the obtained optimum concentration. The protein expression of cysteine-requiring aspartate protease 3（Caspase 3）

B lymphocyte tumor 2（Bcl-2）

Bcl-2-associated X protein（Bax）

and intracellular phosphatidylinositol 3-kinase（PI3 K） was detected

and the nitric oxide（NO） and nitric oxide synthase（eNOS） content were assessed. Results The apoptosis rate of ICC in 10% BXD group was significantly lower than that of blank group and deionized water group（P<0.05）

as well as that of 5% and 15% BXD group（P<0.05）; therefore

10% BXD was selected to be used in the further test. Compared to blank group and deionized water group

the BXD group had higher protein expression of Bcl-2 of ICC

as well as lower protein expression of Caspase-3

BaX and PI3 Kand

and secretion of NO and eNOS（P<0.05）. Conclusion BXD may play role in DGIM through inhibiting the apoptosis of ICC

and the mechanism may be related to its regulation of apoptosis-related proteins including Caspase-3

Bax

PI3 K and Bcl-2

and inhibition of NO and eNOS secretion.