ABSTRACT
ObjectiveTo explore the underlying mechanism of bran-fried Atractylodis Rhizoma （AR） in improving gastrointestinal function by comparing the effects of raw AR and bran-fried AR on the small intestine tissue structure and transport-related protein carriers in rats with spleen deficiency syndrome. MethodSeventy male SD rats were randomly divided into a normal group， a model group， high- and low-dose raw AR groups （10， 2.5 g·kg-1）， high- and low-dose bran-fried AR groups （10， 2.5 g·kg-1）， and a compound glutamine group （9 mg·kg-1）， with 10 rats in each group. Except for the normal group， the other six groups were subjected to the spleen deficiency model induced by the method of bitter and cold breaking stagnated Qi and abnormal hunger and fullness for 21 days. After modeling， each treatment group was given medication orally according to the corresponding doses every day for a total of 14 days， and the normal group and the model group were given an equal volume of normal saline orally. During the treatment period， the general survival status， macroscopic syndrome score， daily increase in body weight and food intake， and rectal temperature of the spleen deficiency rats were evaluated， and after the treatment， the rats were sacrificed. The pathological changes in the small intestine tissues of each group were observed by hematoxylin-eosin （HE） staining. The content of serum 5-hydroxytryptamine （5-HT） was detected by enzyme-linked immunosorbent assay （ELISA）， and the content of serum D-xylose， lactate， and amylase was detected by colorimetry. The levels of free fatty acid receptor 3 （FFA3） and peptide transporter 1 （PepT1） in small intestinal tissues were detected by the Bradford method， and the protein expression of sodium-dependent glucose transporter 1 （SGLT1） and glucose transporter 1 （GLUT1） in small intestinal tissue was detected by immunohistochemistry. Real-time fluorescence-based quantitative PCR was used to detect the mRNA expression of glucose transporter 2 （GLUT2）， sodium/hydrogen exchanger 3 （NHE3）， and 5-hydroxytryptamine receptor 4 （5-HT4R）. ResultCompared with the normal group， the model group exhibited symptoms of spleen deficiency， such as sluggishness， squint， reduced food intake， and lethargy at the end of modelling， damaged basic structure of the small intestinal mucosal epithelium and lamina propria， increased serum lactate and 5-HT content， and decreased serum amylase and D-xylose （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of improvement， with the small intestinal microstructure repaired to different degrees. The daily weight gain， anal temperature， and macroscopic syndrome score of spleen deficiency improved to varying degrees （P<0.05， P<0.01）. The serum lactate and 5-HT content decreased to varying degrees， while the serum amylase and D-xylose content increased to varying degrees （P<0.05， P<0.01）. The PepT1 content in the small intestinal tissues increased， while the FFA3 content decreased to varying degrees. The protein expression of SGLT1 and GLUT1 increased， while the mRNA expression of GLUT2 and NHE3 increased to varying degrees. The mRNA expression of 5-HT4R decreased to varying degrees （P<0.05， P<0.01）. Compared with the high- and low-dose raw AR groups， the high- and low-dose bran-fried AR groups showed significant improvement in general conditions and histopathological improvement of the small intestinal tissues. The daily weight gain， anal temperature， and macroscopic syndrome score of spleen deficiency also improved （P<0.05， P<0.01）. The serum lactate and 5-HT content decreased， while the serum amylase and D-xylose content increased （P<0.05， P<0.01）. The PepT1 content in the small intestinal tissues increased， while the FFA3 content decreased. The protein expression of SGLT1 and GLUT1 increased， while the mRNA expression of GLUT2 and NHE3 increased. The mRNA expression of 5-HT4R decreased significantly （P<0.05， P<0.01）. ConclusionBran-fried AR can improve the spleen deficiency-related symptoms and histopathology of the small intestinal tissues in spleen deficiency model rats. Its mechanism may be related to the regulation of the expression of various transport-related protein carriers and the secretion of various digestive enzymes after stir-frying of AR， thus restoring the absorption and transport function of the small intestine.