CDX2 plays an important role in the development, maintaining shape, structural characteristics of intestinal epithelial cells. Intestinal type gastric cancer is thought to develop a multi-step and multiphase process from normal gastric mucosa,intestinal metaplusia and dysplasia, ultimately to gastric cancer. So far, more and more studies have found that the abnormal expression of CDX2 gene plays an important role in development of intestinal metaplasia, dysplasia and intestinal carcinoma.

AIM To investigate the influences of Astragalus and Hurido effective components on apoptosis of rat glomerular mesangial cells.METHODS The proliferation of rat mesangial cells was induced by LPS and then intervened with Astragalus (astragalus polysaccharide,astragaloside Ⅳ,calycosin) and Hurido (hirudin).The cells were collected after 24 h.4',6-Diamidino-2-phenylindole (DAPI) staining was used to observe cell nuclear changes.Quantitative and qualitative expressions of Bcl-2 were detected by streptavidin-biotin complex (SABC).RESULTS Astragalus and Hurido effective components could induce the apoptosis of rat glomerular mesangial cells,and decrease the expression of Bcl-2.CONCLUSION Astragalus and Hurido effective components can induce the mesangial cell apoptosis by down-regulating Bcl-2 expression,which can be used for the treatment of mesangial proliferative glomerulonephritis.

Objective:To investigate the relationship between hemodynamics with hepatic reserve function in cirrhosis patients complicated with portal hypertension (PHT), and to explore the significances of the two in evaluating the disease.Methods:According to the Child score, 80 cirrhosis patients complicated with PHT from January 2016 to January 2018 in our hospital were divided into three grades: A, B and C, 35 healthy persons in the same period were selected as normal control group. The parameters of liver hemodynamics were detected by color Doppler ultrasound, and the items of liver reserve function were detected by automatic biochemical analyzer. The correlation between hemodynamic indexes and liver reserve function was analyzed by Pearson method, and the risk factors of liver cirrhosis with PHT were analyzed by logistic multiple regression.Results:The diameter of portal inner vein (DPV), maximum speed of blood flow in the portal vein (PVX), mean speed of blood flow in the portal vein (PVM), quantity of blood flow in the main portal vein (QPV), albumin (ALB), cerealthirdtransaminase (ALT), aspartate transaminase (AST) and prothrombin time (PT) in the observation group were significantly higher than those in the control group ( P<0.05), while the total bilirubin (TBIL) was significantly lower than that in the control group ( P<0.05). The levels of DPV, PVX, PVM and QPV in patients with grade C were significantly higher than those in grade A and grade B ( P<0.05); the levels of DPV, PVX, PVM and QPV in patients with grade B of liver function were significantly higher than those in grade A ( P<0.05). The level of TBIL in patients with grade C liver function was significantly lower than that in grade A and grade B patients ( P<0.05); ALB, ALT, AST and PT were significantly higher than those of grade A and grade B ( P<0.05); the level of TBIL in patients with grade B of liver function was significantly lower than that of grade A ( P<0.05), while the ALB, ALT, AST and PT were significantly higher than those in group A ( P<0.05). DPV, PVM and QPV were significantly positively correlated with PT in cirrhosis patients with and PHT ( P<0.05), PVM and QPV were significantly negatively correlated with TBIL ( P<0.05). Regression analysis showed that hemodynamic indexes in DPV, PVX, PVM, QPV and liver reserve function indexes TBIL, ALB, ALT, AST, PT were risk factors for portal hypertension in cirrhosis. Conclusions:Hemodynamics and hepatic reserve function indicators have certain regularity in different degrees of cirrhosis complicated with PHT patients, they are closely related and can be used as an important index in the evaluation and monitoring of cirrhosis with PHT.

ObjectiveTo investigate the protective effect of folic acid against cholestatic liver injury in mice induced by bis（2-ethylhexyl） phthalate （DEHP） exposure and its mechanism. MethodsICR mice were randomly divided into control group， high-dose folic acid （H-FA） group， DEHP group， DEHP+low-dose folic acid （DEHP+L-FA） group， and DEHP+high-dose folic acid （DEHP+H-FA） group， with 6 mice in each group. The mice in the H-FA group， the DEHP+L-FA group， and the DEHP+H-FA group were given folic acid by gavage at the corresponding dose， and those in the control group and the DEHP group were given an equal volume of PBS solution by gavage. After 2 hours， the mice in the DEHP group， the DEHP+L-FA group， and the DEHP+H-FA group were given corn oil containing 200 mg/kg DEHP， and those in the control group and the H-FA group were given an equal volume of pure corn oil， by gavage for 4 weeks. Body weight and food intake were recorded every day， and blood and liver tissue samples were collected. A biochemical analyzer was used to measure the serum levels of total bile acid （TBA） and alkaline phosphatase（ALP）； HE staining was used to observe the histopathological changes of liver tissue； kits were used to measure the content of malondialdehyde （MDA） and superoxide dismutase （SOD） in the liver； LC-MS/MS was used to measure serum bile acid profiles； Western blot was used to measure the expression levels of proteins associated with hepatic bile acid metabolism. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the control group， the daily food intake of the mice in the DEHP group decreased significantly， and the body weight decreased significantly from day 10 （P<0.05）， and compared with the DEHP group， the DEHP+L-FA group and the DEHP+H-FA group had basically unchanged body weight and daily food intake （P>0.05）. Compared with the control group， the DEHP group had significant increases in liver weight index and the serum levels of TBA and ALP （all P<0.05）， with enlarged portal area， bile duct deformity and hyperplasia， and a small amount of inflammatory cell infiltration in liver tissue； compared with the DEHP group， the DEHP+L-FA group and the DEHP+H-FA group had a significant reduction in liver weight index （P<0.01）， and the DEHP+H-FA group had significant reductions in the serum levels of TBA and ALP （P<0.05）， with a significant improvement in liver histomorphology and structure after folic acid intervention. Compared with the control group， the DEHP group had a significant reduction in the content of SOD （P<0.05） and a significant increase in the content of MDA in the liver （P<0.01）， and compared with the DEHP group， the DEHP+H-FA group had significant reductions in the content of MDA and SOD （P<0.05）. Compared with the control group， the DEHP group had significant increases in the serum levels of α-muricholic acid （α-MCA），β- muricholic acid （β-MCA），deoxycholic acid （DCA）， lithocholic acid （LCA）， taurocholic acid （TCA）， taurodeoxycholic acid （TDCA）， tauroursodeoxycholic acid （TUDCA）， tauro-β-muricholic acid （T-β-MCA）， tauro-α-muricholic acid （T-α-MCA）， taurohyodeoxycholic acid （THDCA）， and taurolithocholic acid （TLCA） （P<0.05） and a significant reduction in ursodeoxycholic acid （UDCA）（P<0.05）； compared with the DEHP group， the DEHP+H-FA group had significant reductions in the serum levels of DCA， LCA， TCA， TDCA， TUDCA， T-β-MCA， T-α-MCA， THDCA， and TLCA （P<0.05）. Compared with the control group， the DEHP group had significant increases in the protein expression levels of FXR and CYP3A11 in the liver （P<0.01） and significant reductions in the protein expression levels of CYP7A1 and MRP2 （P<0.01）； compared with the DEHP group， the DEHP+L-FA group and the DEHP+H-FA group had significant reductions in the protein expression levels of FXR and CYP3A11 in the liver （P<0.05） and a significant increase in the protein expression level of MRP2 （P<0.05）， and the DEHP+H-FA group had a significant increase in the protein expression level of CYP7A1 （P<0.05）. ConclusionFolic acid has a protective effect against cholestatic liver injury in mice induced by DEHP exposure， possibly by regulating bile acid synthesis， catabolism， and transport and maintaining bile acid homeostasis.