engleski

The Efficiency of Gallic Acid on Suppression of Angiogenesis, Oxidative Stress and Tumor Growth

Tumor formation is a process that involves accumulation of genetic and epigenetic changes leading to the progressive transformation of normal, healthy cells into malignant. Tumor cells possess certain skills unknown to normal cells: survival, proliferation without dependence on growth factors, unlimited replication, avoidance of apoptosis, invasivnes, metastasis and angiogenesis. The development of tumorogenesis is closely associated with the influence of reactive oxygen species (ROS) at the variety of cellular functions. In the present study we investigated the effect of gallic acid on oxidative stress, tumor growth and angiogenesis in EAT (Ehrlich ascites tumor)- bearing mice. EAT cells (2.5 x 106) were implanted intraperitoneally (i.p.) in Swiss albino mice. After tumor inoculation, mice were injected i.p. with gallic acid (GA) at dose of 40 and 80 mg/kg bw in exponential growth phase from the 5 days after tumor cell injection (on day 5, 7, 9, 11). On day 13, ascites volume, the total number of cells, differential count of the cells present in the peritoneal cavity, functional activity of macrophages, anti-angiogenic and antioxidant parameters were determined. Results show that GA inhibited the growth of EAT cells and the formation of ascites in the peritoneal cavity of EAT-bearing mice. Further, results on decrease in the peritoneal angiogenesis and microvessel density show the anti-angiogenic potential of GA in vivo. Gallic acid also decreased nitric oxide (NO) level in tumor cells whereas NO level was increased in peritoneal macrophages. Decreased level of Arginase 1 (ARG 1) indicate that polarization is prevented in M2 macrophages. Based on the results we can conclude that the GA can activated macrophages and increase their cytotoxic activity through increased production of NO and prevent tumor growth and angiogenesis.

oxidative stress, gallic acid, angiogenesis, tumor

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