Objective To provide a comprehensive review of the modeling method of the empty bottle stimulation(EBS)anxiety model,including commonly used experimental animal strains and genders,animal grouping,modeling procedures,modeling duration,primary behavioral evaluation method,and the underlying pathological mechanisms.This aims to offer a reference for the application of the EBS anxiety model in anxiety disorder research.Methods Searches were conducted in databases such as CNKI and PubMed to collect all literature related to the EBS anxiety model,which were then systematically summarized and organized.Results(1)Male adult SD or Wistar rats are predominantly used as experimental animals;(2)The optimal modeling period is 2 weeks;(3)Behavioral evaluations primarily utilize the open field test,elevated plus maze test,and light-dark box test;(4)Pathological mechanisms involve abnormal neurotransmitter metabolism in brain regions such as the hippocampus,prefrontal cortex,and amygdala.Conclusions The EBS anxiety model exhibits an anxiety-like behavioral phenotype and associated neurobiological mechanisms,validating its utility as an animal model for the study of anxiety disorders.However,further exploration and refinement are required for its standardized construction protocol and the understanding of its mechanistic underpinnings.

Objective To provide a comprehensive review of the modeling method of the empty bottle stimulation(EBS)anxiety model,including commonly used experimental animal strains and genders,animal grouping,modeling procedures,modeling duration,primary behavioral evaluation method,and the underlying pathological mechanisms.This aims to offer a reference for the application of the EBS anxiety model in anxiety disorder research.Methods Searches were conducted in databases such as CNKI and PubMed to collect all literature related to the EBS anxiety model,which were then systematically summarized and organized.Results(1)Male adult SD or Wistar rats are predominantly used as experimental animals;(2)The optimal modeling period is 2 weeks;(3)Behavioral evaluations primarily utilize the open field test,elevated plus maze test,and light-dark box test;(4)Pathological mechanisms involve abnormal neurotransmitter metabolism in brain regions such as the hippocampus,prefrontal cortex,and amygdala.Conclusions The EBS anxiety model exhibits an anxiety-like behavioral phenotype and associated neurobiological mechanisms,validating its utility as an animal model for the study of anxiety disorders.However,further exploration and refinement are required for its standardized construction protocol and the understanding of its mechanistic underpinnings.

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.

OBJECTIVETo investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro.

METHODSHuman airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10(-8) mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA.

RESULTS16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58).

CONCLUSIONBoth 1,25VD3 and HDM can induce TSLP expression and release in 16HBE cells, but pretreatment with 1,25VD3 can decrease HDM-augmented TSLP expression in the cells.

Animals ; Bronchi ; cytology ; Calcitriol ; pharmacology ; Cell Line ; Cytokines ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; Humans ; Pyroglyphidae

Objective To investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro. Methods Human airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10-8 mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA. Results 16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58). Conclusion Both 1,25VD3 and HDM can induce TSLP expression and release in 16HBE cells, but pretreatment with 1,25VD3 can decrease HDM-augmented TSLP expression in the cells.

Objective To investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro. Methods Human airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10-8 mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA. Results 16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58). Conclusion Both 1,25VD3 and HDM can induce TSLP expression and release in 16HBE cells, but pretreatment with 1,25VD3 can decrease HDM-augmented TSLP expression in the cells.