Objective To investigate whether curcumin could inhibit the metastasis of pancreatic cancer in vitro and in vivo and its mechanism.Methods Pancreatic cancer AsPC-1 cells were treated with different concentrations of curcumin.After 72 hours,cell survival rate were detected by MTT and the appropriate concentration of curcumin was selected.After treated with 6 μmol/L curcumin,early apoptosis of AsPC-1 cells were detected by Annexin V-FITC/PI double staining flow cytometry,and the effects of curcumin on the migration and invasion of AsPC-1 cells were observed.After establishment of the orthotopic nude mouse model of pancreatic cancer,the mice were orally treated with low dose (20 mg/kg body weight) and high dose (40 mg/kg body weight) of curcumin respectively.Eight weeks later mice were sacrificed to observe the tumor metastasis,immunohistochemical methods were used to detect the positive expressions of CD34,NF-κB and MMP-9 in the tumor tissue.Results Curcumin of different concentrations could inhibit the proliferation of AsPC-1 cells and induce its apoptosis in a dose dependent manner,and 6.μmol/L was the best dose of curcumin.After 6 μmol/L curcumin treatment,the migration coverage of AsPC-1 decreased from 70％ to 10％,the number of penetrating cells decreased from 136/200x magnification to 17/200x magnification,and the difference between the two groups was statistically significant (P ＜0.05).In the nude mouse model of pancreatic cancer,the size of the tumor decreased from (97.8 ± 15.3) mm3 to (44.3 ± 9.7) mm3 in high dose group and (28.1 ±7.1)mm3 in low dose group,the number of distant metastasis decreased from 108.3 ±6.7 to 29.5 ±4.5 and 8.9 ± 2.4,the expression of CD34 decreased from 20.5 ± 2.3 to 10.3 ± 1.2 and 7.9 ± 3.2,and the expression of MMP-9 decreased from 85.2 ± 2.3 to 53.2 ± 1.2 and 34.2 ± 3.1,and the difference was statistically significant (P ＜ 0.05).Conclusions Curcumin can inhibit the metastasis of pancreatic cancer both in vitro and in vivo,and its effect may be related to the inhibition of expressions of CD34 and MMP-9.

Objective To investigate the protective effects of (-)-epigallocatechin gallate ( EGCG ) on daunorubicin ( DNR)-induced cardiotoxicity in mice. Methods The qualified mice were randomly divided into four groups:normal control group, myocardial injured model control group,high dose group (80 mg·kg-1 ) and low dose group (40 mg·kg-1 ) of EGCG. EGCG was administered intragastrically once daily for 7 days,followed by a single intraperitoneal injection of DNR (15 mg·kg-1 ) except in the normal control group. The electrocardiogram,myocardial enzymes and TNT-Hs in serum,cardiac ultrastructure of mice were detected after 48 h. Results In DNR model control group,the incidence of arrhythmia was 64. 7%. The activity of serum cardic enzymes including CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs were significantly higher than those in the normal control group(P<0. 01),and myocardial ultrastructure was injured remarkably. The incidence of arrhythmia was 44. 4% in mice treated with high dose of EGCG and 31. 6% in mice with low dose of EGCG. Compared to the model control group, the activity of CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs in serum decreased remarkably in EGCG groups( P<0. 05 or P<0. 01). Low can EGCG alleviated the injury to the ultrastructure of myocardium compared to the model control group. Conclusion EGCG can prevent the cardiac toxicity induced by DNR in mice.

Objective To explore the influence of LPS treatment on related molecules in Smads and ERK1/2 signal pathway in pancreatic stellate cell line LTC-14.Methods LTC-14 cells were cultured in vitro, and were treated with LPS at different dose in different time points.Protein expressions of related molecules in Smads pathway and ERK1/2 pathway and α-SMA in LTC-14 Cells were examined by Western blot.Results On Treated LTC-14 cells by 0, 1, 5, 10, 20 and 50 mg/L LPS,protein expressions of Smad3 were 0.15±0.02, 0.37±0.02, 0.44±0.01, 0.46±0.02, 0.372±0.01 and 0.24±0.03;expressions of Smad7 were 0.79±0.05, 0.84±0.02, 0.55±0.03, 0.45±0.03, 0.34±0.02 and 0.92±0.07;p-ERK1/2 levels were 0.48±0.05, 0.74±0.03, 0.72±0.04, 0.89±0.02, 0.81±0.02 and 0.72±0.03;p-cPLA2 levels were 0.15±0.03, 0.30±0.01, 0.31±0.01, 0.30±0.02, 0.28±0.03 and 0.32±0.02;α-SMA levels were 0.56±0.06, 0.62±0.06, 0.54±0.04, 1.03±0.11, 1.39±0.08 and 1.28±0.10.The changes of protein expressions before and after LPS treatment were obvious (all P<0.01).The protein expressions of ERK1/2 were 0.56±0.03, 0.57±0.02, 0.53±0.02, 0.58±0.02, 0.59±0.05 and 0.55±0.04, which did not change obviously along with increased LPS dosages.LTC-14 cells treated with 10 mg/L LPS for 0, 1, 3, 6 and 9 h,the expressions of Smad3 were 0.69±0.05, 0.68±0.07, 1.02±0.14, 1.82±0.0 and 2.04±0.11,those of Smad7 were 2.77±0.10, 1.37±0.08, 1.45±0.14, 0.78±0.09 and 0.63±0.06,those of p-ERK1/2 were 0.16±0.03, 0.32±0.05, 0.79±0.03, 1.50±0.07 and 1.77±0.04,those of p-cPLA2 were 0.15±0.04, 0.32±0.06, 0.63±0.04, 0.95±0.04 and 1.49±0.10,those of α-SMA were 0.84±0.03, 1.26±0.21, 1.81±0.19, 4.28±0.26 and 4.37±0.15, all of which changed obviously as the treatment time increased (P<0.05 or 0.01).The expressions of ERK1/2 were 0.75±0.03, 0.72±0.02, 0.80±0.04, 0.74±0.03 and 0.85±0.09, which did not change obviously as the treatment time increased.Conclusions LPS could upregulate the expression of α-SMA in a time-and dose-dependent way, and activate intracellular Smads and ERK1/2 inflammatory pathways, which may be the potential molecular mechanism of the development of chronic pancreatitis.

Objective:To investigate the characteristics of implicit memory and its related factors in schizophrenic patients with negative and positive symptoms.Methods:Ninety-three schizophrenic patients (including 52 cases of negative symptoms group and 41 cases of positive symptoms group) and 30 normal controls (normal group) were tested with the method of Chinese character word completion method. The reaction time and correct rate were recorded and compared with analysis of variance and t-test, and the correlation with demographic factors was analyzed with Pearson correlation analysis. Results:Accuracy of implicit memory test in schizophrenia group: there were statistically significant differences in the accuracy of patients with different course of disease (≤5 years: (38±5)%, 5-15 years: (34±8)%, ≥15 years: (34±7)%, P<0.05).The differences were statistically significant in the accuracy of patients with different education levels(primary school: (35±6)%, junior and senior high school: (34±7)%, secondary college education and above: (39±5)%, P<0.05).The accuracy of patients with education years < 10 years ((34±7)%) was significantly lower than those with education years ≥10 years ((37±6)%, P<0.05).Reaction time results of implicit memory test in schizophrenia group : there were significant differences in reaction time of patients with different disease course(≤5 years: (3 248±971)ms, 5-15 years: (3 515±672)ms, ≥15 years: (3 925±842)ms, P<0.05).The differences were statistically significant in the reaction time of workers ((3 495±712)ms), farmers ((3 870±878)ms) and soldiers ((3 024±924)ms, P<0.05).The reaction time of patients with clozapine ((3 869±871)ms) was significantly higher than that of patients with olanzapine ((3 393±626)ms, P<0.05).Intergroup results of accuracy: the accuracy of normal control group ((40±5)%) was significantly higher than that of negative symptom group ((33±7)%, P<0.01).The accuracy of negative symptom group was significantly lower than that of positive symptom group ((37±6)%, P<0.01).Intergroup reaction time results: the reaction time of normal control group ((2 660±667)ms) was significantly lower than that of negative symptom group ((3 678±951)ms, P<0.01) and positive symptom group ((3 072±865)ms, P<0.05).The reaction time of negative symptom group ((3 678±951)ms)was significantly higher than that of positive symptom group( P<0.01).There was significant negative correlation between the accuracy of implicit memory and the course of disease in schizophrenia ( r=-0.22, P<0.05). Conclusion:The implicit memory of schizophrenic patients is related to the course of disease, taking drugs, and occupation.There may have differences in implicit memory between patients with negative and positive symptoms of schizophrenia.