| Growth and metastasis of malignant tumor depends on angiogenesis. Vessel of tumor is the morphology foundation for growth and metastasis of malignant tumor. The vessel of tumor not only provide tumor with nutrients, but also it deliver tumor cells to other place in human body. This leads to growth and metastasis of malignant tumor. It is well known at present that the growth of tumor has two distinctive stages: one is avascular stage and another is vascular stage. The former depends on diffuse oxygen supplied. The oxygen's diffuse distance is no more than 150μm. When tumor's diameteris more than wo to three mm, Its succeed growth needs blood supplied. As a result, antiangiogenesis is a effective new way during clinical treatment of tumor. It is a target to aim at the every linking of angiogenesis. To develop angigogenesis inhibitor may be an important way to control the growth and matastasis of tumor. Lung cancer is one of the common malignant tumor and it threaten health and life of human. Lung cancer has the same general character as other solid tumor. The characteristic of lung cancer is that its structure is complex and its vessel is more affluence . Study indicated that occurrence, progress and metastasis of lung cancer and carcinoma metastaticum is the ideal pattern. Angiogenesis of lung cancer will open up a new way for treatment of lung cancer. Up to now, the treatment of lung cancer is not satisfated yet. Searching after new programme becomes very necessary in order to heighten the cure ratio and the quality of life. Study indicated that thalidomide had the action of antitumor which was related with antiangiogenesis. The mechanism of anti-angiogenesis of thalidomide in solid tumor is not formed systemical theory. The mechanism has not been completely understanded. In present, we have investigated the mechanism of thalidomide inhibiting the growth and metastases of tumor by measuring their antiangiogenic effects.Objective:To investigete the mechanism of thalidomide regulating angiogenesis of lung cancer, thus title may provide the treat ment of lung cancer with new route of research. Methods:⒈Human umbilical vein endothelial cells line ECV304 and human lung cancer cells line SPC-A-1 were cultured in RPMI1640, and therapy group were given thalidomide with or without liver microsomes of rabbit at several concentrations, the cell inhibition rate were evaluated by MTT method.⒉Supernatant liquid of SPC-A-1 cells pretreated with thalidomide groups was collected and the activity of gelatinase was measured by Zymgraphy. ⒊SPC-A-1 cell total protein pretreated with therapy groups was extracted after twenty-four hours, and their bFGF and MMP-2 level was measured by Western blot method.⒋Chick chorioallantoic membranes(CAM) was adopted to estimate the effects of thalidomide on angiogenesis.⒌Rat model of Lewis lung cancer was established, treated with different doses of thalidomide, normal saline and TNP470 as negative and positive factor, masses of tumor were weighed, bFGF and MMP-2 , MVD were detected by immunohistochemistry, the level of bFGF and MMP-2 was examined by Western Blot method.Result:⒈When thalidomide's concentration was 0.8,8 or 80μg/ml with or without liver microsomes, there were no significant difference between therapy group and control for proliferation of SPC-A-1 cells (P>0.05).⒉When thalidomide's concentration was 0.8,8 or 80μg/ml without liver microsomes, there was no significant difference between therapy group and control for proliferation of ECV304 and angiogenesis of CAM (P>0.05).⒊When thalidomide's concentration was 8 or 80μg/ml with liver microsomes, there was significant difference between therapy group and control or between therapy groups for proliferation of ECV304 and angiogenesis of CAM (P<0.05).⒋ When thalidomide's concentration was 8 or 80μg/ml without liver microsomes, the ratio of activity of MMP-2 and MMP-9 compared with the control was almost equal. When thalidomide's concentration was 8 or 80μg/ml with liver microso... |
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