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1.
Asian Pacific Journal of Tropical Medicine ; (12): 473-477, 2014.
Article in English | WPRIM | ID: wpr-820668

ABSTRACT

OBJECTIVE@#To analyze expression heterogeneity of Integrin beta 3 (ITGB3) and B-cell lymphoma 2 (BCL-2) in lung adenocarcinoma tissue and adenocarcinoma cell line and further provide theoretical direction for molecular biological research of lung adenocarcinoma.@*METHODS@#Tissue microarray was used to observe relation among expression, heterogeneitpy and clinical characteristics of ITGB3 and BCL-2 in lung cancer.@*RESULTS@#ITGB3 and BCL-2 increased significantly in A549 cells in CAFs group withβ-actin as control; the expression level of BCL-2 also increased in ITGB3 transfected cells with GFP plasmid transfected A549 cells as control; immunohistochemistry staining showed that positive rates of ITGB3, ITGB1 and BCL-2 in normal lung tissues were 0, the positive rates in lung adenocarcinoma were 7.04%, 84.51% and 4.23%, respectively; in the results of immunohistochemistry staining, the expression of Girdin protein in lung adenocarcinoma was homogeneous, however protein expression of ITGB3, ITGB1 and BCL-2 showed different patterns in the same location with significant heterogeneity; majority of ITGB3, ITGB1 or BCL-2 positive tissue showed heterogeneity that expression in trailing edge was higher than that of trailing edge in lung adenocarcinoma tissue, the patients with BCL-2 heterogeneity showed higher lymph node metastasis ratio and lower clinical stage (P0.05).@*CONCLUSIONS@#Expression of ITGB3 and BCL-2 in lung adenocarcinoma and adenocarcinoma cell line showed heterogeneity that expression in trailing edge was higher than that of trailing edge, which may play an important role in promoting tumor lymph node metastasis and vascular invasion, and provides a new research direction for exploration of lung adenocarcinoma metastasis mechanism.


Subject(s)
Humans , Adenocarcinoma , Chemistry , Metabolism , Adenocarcinoma of Lung , Cell Line, Tumor , Integrin beta3 , Genetics , Metabolism , Lung , Chemistry , Metabolism , Lung Neoplasms , Chemistry , Metabolism , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Tissue Array Analysis , Transfection
2.
Journal of Central South University(Medical Sciences) ; (12): 54-58, 2007.
Article in Chinese | WPRIM | ID: wpr-813937

ABSTRACT

OBJECTIVE@#To explore the effect of extract of ginkgo biloba leaves on the precondition of liver graft in rat liver transplantation.@*METHODS@#Male Sprague-Dawley rats were used as donors and recipients of orthotopic liver transplantation (OLT), and were randomly divided into extract of ginkgo biloba leaves group (Egb), NS control group (NS), and sham operation group (SO) according to whether the extract of ginkgo biloba leaves was injected by the venous (40 mg/kg) 1 h before the liver grafts harvesting. The rats were killed at 2 h, 6 h, and 24 h after the ischemia/reperfusion. The serum concentrations of ALT and AST were determined and the liver tissue were sampled to observe the expression of TNF-alpha and IL-1.@*RESULTS@#After the ischemia/reperfusion the serum concentration of ALT and AST and expressions of TNF-alpha and IL-1 in the hepatic tissue in the NS group significantly increased (p<0.01), and the hepatocytic morphologic change was obvious compared with the SO group. The treatment of ginkgo biloba extract significantly decreased the serum concentration of ALT and AST and the expressions of TNF-alpha and IL-1 in the hepatic tissue in EGb group compared with the NS group (p<0.01), and relieved the hepatocyte swelling and necrosis.@*CONCLUSION@#Ginkgo bilobA extract may decrease the release of TNF-alpha and IL-1 by inhibiting activation of kuffer cells and regulate the cell factors to protect the live.


Subject(s)
Animals , Male , Rats , Alanine Transaminase , Blood , Aspartate Aminotransferases , Blood , Drugs, Chinese Herbal , Pharmacology , Ginkgo biloba , Chemistry , Interleukin-1 , Liver , Metabolism , Liver Transplantation , Plant Leaves , Chemistry , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury , Blood , Metabolism , Tumor Necrosis Factor-alpha
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