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1.
Chinese Journal of Pancreatology ; (6): 38-42, 2019.
Article in Chinese | WPRIM | ID: wpr-744124

ABSTRACT

Objective To explore the effect of Kruppel like factor 4 (KLF4) on epithelial-to-mesenchymal transition and invasion ability of pancreatic cancer.Methods The expression of KLF4 in 70 pancreatic cancer tissues and 10 normal pancreatic tissues was detected by immunohistochemistry,and the correlations between KLF4 expression and pathological characteristics were analyzed.Small hairpin RNA targeting KLF4 (sh-KLF4) and negative control shRNA were constructed.After the transfection of shRNA,qRT-PCR and western blot were used to detect the mRNA and protein expression of KLF4,E-cadherin and vimentin,and cell scratch-wound assay and transwell assay were utilized to determine the ability of invasion and metastasis.Results KLF4 expression (47.1%) was lower in pancreatic cancer tissues compared with normal pancreatic tissues (80.0%),and negatively correlated with cell differentiation,tumor stage and distant metastasis.Down-regulated KLF4 expression in PANC1 cell caused decreased mRNA and protein expression of E-cadherin (F =25.71,P =0.0011) and increased mRNA and protein expression of vimentin (F =24.95,P=0.0012).Knockdown of KLF4 in PANC1 cell promoted the transition from epithelial morphology to mesenchymal morphology,and enhanced the healing ability (F =47.82,P < 0.001),migration (F =53.68,P=0.0001) and invasion (F=27.65,P=0.0009).Conclusions Knockdown of KLF4 can promote EMT and enhance the invasion ability of pancreatic cancer.

2.
China Pharmacy ; (12): 2855-2858, 2017.
Article in Chinese | WPRIM | ID: wpr-616260

ABSTRACT

OBJECTIVE:To improve community pharmaceutical care so as to promote the rational drug use of community resi-dent and improve the quality of life. METHODS:By analyzing the situation of community pharmaceutical care,the pharmaceutical care of community pharmacists was improved by changing pharmaceutical care mode,actively developing the propaganda of ratio-nal drug use,strengthening retraining of clinical pharmacists. RESULTS:With the help of Hongkou district quality control group, many hospitals of the district signed thepharmaceutical linkage assistance agreement. Through the efforts of Hongkou district quality control group and many hospitals,community pharmaceutical care was improved and the propaganda of rational drug use has achieved certain results. CONCLUSIONS:Through exploration and practice,the pharmaceutical care levels of community phar-macists have been improved and the rational drug use of community residents has been promoted.

3.
The Journal of Practical Medicine ; (24): 2440-2442, 2015.
Article in Chinese | WPRIM | ID: wpr-477654

ABSTRACT

Objective To evaluate the effect of sufentanil postconditioning on myocardial ischemia-reperfusion injury in rats, and to investigate the possible mechanism. Methods Thirty male Sprague-Dawley ratswere randomly divided into 5 groups (n = 6 each): sham group (group S), I/R group (group I/R), low dose of sufentanil postconditioning group (group SL), high dose of sufentanil postconditioning group (group SH) andsufentanil postconditioning plus wortmannin group (group WM). Different drugs were injected before reperfusion: normal saline (NS) and sufentanil 1 μg/kg in group SL, NS and sufentanil 3 μg /kg in group SH, wortmannin 15 μg/kg andsufentanil 1 μg/kgin group WM, and NS in group S and I/R. At the end of reperfusion, artery blood was collected for assessment of plasma cTnI concentration; And the heart was harvested for determination of infarct size (IS) and area at risk (AAR). Results Compared with group S, cTnI concentration was increasedin the rest groups (P< 0.01); Compared with group I/R, cTnI concentration was decreased in group SL, SH and WM, while IS/AAR reduced in group SL and SH (P < 0.01); Compared with group SL, cTnI concentration and IS/AAR were decreased in group SH while increased in group WM (P <0.01). Conclusion Sufentanil postconditioning could attenuate myocardial ischemia-reperfusion injury in rats, and the mechanism involved PI3K related pathway.

4.
Chinese Journal of Pancreatology ; (6): 91-94, 2014.
Article in Chinese | WPRIM | ID: wpr-447816

ABSTRACT

Objective To investigate the effect and mechanism of STAT3 gene silencing on the growth of xenografts in human pancreatic cancer SW1990 cells in nude mice.Methods The expression vector inserted with shRNA targeting at STAT3 gene was constructed and was stably transfected into SW1990 cells (SW1990-RNAi group).SW1990 cells transfected with negative control shRNA expression vector (SW1990-Con group) and parent SW1990 (SW1990 group) were used as controls.STAT3,VEGF,MMP-2 protein expressions in these groups were determined by using Western blot.The subcutaneous xenografts models were established in nude mice,and the growth of xenografts was observed,CD34 expressions were determined by immunohistochemistry and MVD was measured.Results The expression of STAT3 protein was 84.69 ± 9.31,82.00 ± 7.76,7.93 ± 1.24,repectively,in SW1990 group,SW1990-Con group,SW1990-RNAi group,and the expression of VEGF protein was 82.94 ± 8.97,80.86 ± 10.28,39.04 ± 6.23,respectively,and the expression of MMP-2 protein was 40.88 ± 5.09,38.26 ± 5.71,12.54 ± 2.15,respectively.The expression in SW1990-RNAi group was significantly lower than those in other 2 groups (P < 0.05),while the expression of all three proteins between SW1990-Con group and SW1990 group was not significantly different.The weight of the xenografts in SW1990 group,SW1990-Con group,SW1990-RNAi group was (2.2 ± 0.4),(2.2 ± 0.3),(0.5 ± 0.3) g,respectively ; the MVD of the xenografts was (20.35 ± 2.41),(18.79 ± 1.94),(9.62 ± 1.06) per high power field,respectively,and the number in SW1990-RNAi group was significantly lower than those in other 2 groups (P < 0.05 or P < 0.01),while the difference between SW1990-Con group and SW1990 group were not significant.Conclusions Inhibition of STAT3 gene expression can significantly slow the growth of SW1990 xenografts in nude mice,and the mechanism may be related with down-regulation of VEGF and MMP-2 expression and inhibition of the angiogenesis of pancreatic cancer.

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