OBJECTIVE To investigate the pharmacodynamic effects of the Citri Grandis Exocarpium extract on anorexia model immature rats.METHODS Ten immature rats were randomly selected as the control group and given regular diet， while anorexia model was induced in the remaining 50 immature rats using the etiological simulation method. The immature model rats were divided into the model group， Jianwei xiaoshi tablet group （0.65 g/kg）， Citri Grandis Exocarpium extract low-dose， medium- dose and high-dose groups （0.5， 1.0， 2.0 g/kg）. After 14 d of continuous intragastric administration， the body mass and food intake of rats in each group were observed， and the gastric acid concentration， pepsinase activity， serum levels of gastrin （GAS）， motilin （MTL） and gastric inhibitory peptide （GIP） were measured. The histopathological changes in the gastric tissue were observed.RESULTS Compared with control group， the food intake， gastric acid concentration， pepsin activity， the levels of GAS and MTL were significantly decreased and GIP level was significantly increased in the immature rats of model group （P＜0.05）； gastric histopathological examination showed significant gastric mucosal congestion and loosening and detachment of epithelial cells. Compared with model group， all administration groups showed different degrees of improvement in the above indexes and decreased gastric histopathological damage after drug intervention.CONCLUSIONS Citri Grandis Exocarpium extract improves gastric motility and protects gastric mucosa in the immature rats by regulating the concentration of gastric acid， pepsin activity， the levels of GAS， MTL and GIP， thus improving anorexia in immature rats.

ObjectiveTo explore the pharmacodynamic effect of the water extract of Citri Grandis exocarpium （WEC） on mice with alcohol-induced acute liver injury and provide data support for the development of this medicinal for anti-alcoholism and liver protection. MethodThe main components of WEC were determined by high performance liquid chromatography （HPLC）. Sixty Balb/c mice were randomized into 6 groups： control group （equal volume of 0.5% carboxymethyl cellulose sodium solution）， model group （equal volume of 0.5% carboxymethyl cellulose sodium solution）， low-， medium-， and high-dose WEC groups （0.5， 1.0， 2.0 g·kg^-1）， and Haiwang Jinzun tablet positive control group （2.0 g·kg^-1）. The administration lasted 14 days. One day before the end of the administration， mice were fasted for 12 h with free access to water. The mice， except the control group， were given 56° Chinese liquor （13 mL·kg^-1）. After 2 h， blood was taken from eyeballs and the liver was dissected and weighed. Automatic biochemical analyzer was employed to detect the expression of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， and alcohol dehydrogenase （ADH）. The pathological changes of liver tissues were observed based on hematoxylin-eosin （HE） staining， and apoptosis of hepatocytes based on TUNEL/DAB staining. The expression of proteins related to apoptosis was detected by Western blot. ResultAccording to the HPLC fingerprint， the main components of WEC were rhoifolin and naringin. Compared with the control group， the model group showed increase in liver/body weight ratio （P<0.01） and the expression of ALT and AST （P<0.05， P<0.01）， decrease in the expression of ADH （P<0.05）， blurred structure of hepatic lobules， pathological changes of liver tissue， loose cytoplasm with edema， severe steatosis， rise of the TUNEL-positive rate （P<0.01）， reduction in expression of Bcl-2 （P<0.01）， and increase in Bax and Caspase-3 （P<0.01）. Compared with the model group， medium-dose WEC lowered liver/body weight ratio （P<0.05）. All doses of WEC depressed the activity of ALT and AST （P<0.05， P<0.01）， up-regulated the expression of ADH （P<0.05）， significantly improved the pathological features of alcohol-induced cytoplasmic porosity， edema， and steatosis， down-regulated the TUNEL-positive rate （P<0.05， P<0.01）， enhanced the expression of Bcl-2 （P<0.05）， and decreased Bax and Caspase-3 （P<0.01）. ConclusionWEC regulates the expression of ALT， AST， and ADH and improves hepatic steatosis and hepatocyte apoptosis to fight against acute liver injury.