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Objective: As early as in 1971, Folkman proposed a view of tumor growth and metastasis are dependent on angiogenesis. Clinical and animal experiments confirmed that, if there is no formation of new blood vessels, tumor diameter or thickness of the stop growing after 1 ~ 2mm. The study found that tumor cells can produce vascular endothelial growth factor, can be induced by a variety of anti-angiogenic factor production; tumor vascular growth factor effect is greater than the anti-vascular endothelial growth factor role in accelerated tumor growth, metastasis or recurrence. Inhibition of tumor angiogenesis can prevent tumor growth, metastasis, or recurrence. Currently, a variety of anti-tumor vascular generation drug has been used clinically, and a variety of malignant tumor patients benefit. Renin - angiotensin system (RAS), a biologically active peptide angiotensin Ⅱ (Ang Ⅱ), plays an important role in the regulation of cardiovascular function and water and electrolyte balance; clinical and animal studies show that: Ang Ⅱ has promote the role of tumor cell proliferation and tumor angiogenesis. Of angiotensin II receptor (AT1R) antagonist candesartan inhibition of tumor angiogenesis favor of tumor growth, metastasis, recurrence mechanism conducive to investigate the treatment of advanced malignancies, is conducive to tumor vascular target to the research and development of drugs. Methods: random 50 BALB / C male mice were divided into five groups: saline group (NEC blank control group, at room temperature 0.9% NS 0.6ml / only), low-dose candesartan group (LCA 50mg/day / kg), medium dose candesartan group (MCA 100mg/day/kg) of high-dose candesartan group (HCA 200mg/day/kg) and fluorouracil group (2.5% 5-FU, 25mg/day / kg). Establishment of experimental animal models of liver cancer after successful modeling of 5 mice implementation of interventions; NEC blank control group applications around 10:00 0.6ml / room temperature 0.9% NS gavage once a day for eight consecutive days; LCA, MCA, HCA experimental group around 10:00 daily application 50mg/day/kg, 100mg/day/kg 200mg/day/kg room temperature the Candesartan solution gavage once daily for 8 consecutive days; 5 - FU group around 10:00 daily application at room temperature 2.5% 5-FU solution by intraperitoneal injection for six consecutive days. Before the experiment, the experiment was measured before the administration of 2,4,6,8 body weight of mice, experiment 9 Day, all off of the mice in each group were sacrificed, surgical complete reversal of the tumor tissue, and weighed, Reversal of tissue decile cut, respectively, 10% formalin-fixed (to prepare HE staining and immunohistochemistry, observed tumor tissue AT1-positive rate and MVD), 4% glutaraldehyde (for transmission electron microscopy). Result: 1.NEC blank control body weight of mice is increasing day by day, the average weight of the mice of the 8th after the experiment was 20.85 ± 1.34 g. The rest of the group of mice body weight daily decreased to varying degrees, the average weight of the mice in each group of 8 days after the experiment were: 17.13 ± 2.89 g (HCA), 18.53 ± 2.01g (MCA), 19.44 ± 1.60g (LCA), 15.75 ± 2.63g (5-FU). Results of analysis of variance showed that: The differences between groups were significant (P lt; 0.05); Tip: The weight of the mice decreased with increasing dose of candesartan. The end of the experiment, application count statistics test among the groups of mice survival quality score, results show that: the quality of life of each group mice there were significant differences (P lt; 0.05); Tip: With the candesartan dose increased continuously improve the quality of life in mice. The end of the experiment, mice tumor volume were 233.66 ± 1.62mm3 (NEC),, 144.74 ± 1.21mm3 (HCA), 149.18 ± 88.72mm3 (MCA), 238.63 ± 1.42mm3 (LCA) and 69.05 ± 41.87mm3 ( 5-FU), analysis of variance showed: The differences between groups were significant (P lt; 0.05); Tip: mouse tumor volume decreased with the increase in the dose of candesartan. 4. Between the groups after the end of the experiment, mice tumor weight were 0.9462 ± 0.12 g (NEC), .5193 ± 0.12 g (HCA), .6009 ± 0.15g (MCA), .8450 ± 0.18 g (LCA), 0.5347 ± 0.05g (5-FU), variance analysis results show that: the differences between groups were significant (P lt; 0.05); Tip: mouse tumor weight decreased with the increase in the dose of candesartan. The end of the experiment, average microvascular density (MVD) in tumors of mice in each group were 11.70 ± 2.63 (NEC), (HCA), 4.80 ± 0.92, 7.30 ± 1.06 (MCA), 7.60 ± 0.84 (LCA) 10.90 ± 1.37 (5-FU), analysis of variance showed: The differences between groups were significant (P lt; 0.01); Tip: (1) within the mouse tumor MVD decreased with increasing dose of candesartan; candesartan (2) losartan can curb tumor growth by inhibiting tumor angiogenesis, the mechanism of action of 5-FU. 6 after the experimental application count statistics test the extent of tumor the AT1R the expression between the groups of mice, the results show that: the differences between groups were significant (P lt; 0.05). Tip: candesartan anti-tumor effect is achieved through AT1R. The ultrastructure of the tumor cells of mice in each group. TEM study of the end of the experiment, the results show that: the groups were seen in varying degrees of disintegration and necrosis of tumor cells, the cell membrane is incomplete. Conclusion: AT1R antagonist (candesartan) can significantly inhibit the growth of mice transplanted liver, inhibition of angiogenesis, reduce AT1R expression, improve the quality of life in mice; candesartan role may come through AT1R achieve. The results of this study again confirmed: candesartan can be used as a new anti-angiogenic drugs.
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