High dose gabapentin does not alter tumor growth in mice but reduces arginase activity and increases superoxide dismutase, IL-6 and MCP-1 levels in Ehrlich ascites.

OBJECTIVES: The purpose of this study was to evaluate the effect of gabapentin on Ehrlich tumor growth in Swiss mice, a highly aggressive and inflammatory tumor model. Mice were grouped into sets of 5 animals and treated from days 2 to 8 with gabapentin 30 mg/kg body weight (G30) or 100 mg/kg body weight (G100), or normal sterile saline (control). RESULTS: The mice were euthanized on day 10. Tumor growth, tumoricidal agents and inflammatory cytokines levels were assessed. At day 10, G30 and G100 mice gained weight, but there were no differences in tumor cell count or in ascites volume. In G100, there was a reduction in arginase and an increase in SOD activities. There was an increase in IL-6 and MCP-1 levels, especially in G100, but no alterations in TNF-α. There was no direct evidence of tumor induction by gabapentin. However, the findings suggest that its use modulates immune response to a more effector and less deleterious profile, with increase in activity of anti-oxidant enzymes and in cytokines that favor activation of macrophages, which could improve the general status of the tumor host.

Tumor growth activity of duloxetine in Ehrlich carcinoma in mice.

OBJECTIVE: The objective of this study was to analyze whether duloxetine influences tumor growth in Ehrlich carcinoma. The mice were administered 5 or 30 mg/kg of duloxetine or saline solution. All animals were inoculated with tumor cells. The tumor progression was evaluated by body weight, abdominal circumference, ascites volume and tumor cell count. The effect of duloxetine on immune response was evaluated by lymphoid cells, nitric oxide (NO) production, arginase and superoxide dismutase (SOD) activity and the spleen immunophenotyping. RESULTS: There was no difference between the groups regarding weight, abdominal circumference, ascites volume and number of tumor cells. Duloxetine increased the cells of the inguinal lymph node. There was no difference in the number of cells in the bone marrow and spleen. Ascites SOD activity was greater in Duloxetine groups. There were no differences in the levels of NO, nitrite, and arginase. The number of antibody for CD3 (CD3+), CD4+, CD8+ and CD28+ cells was lower in the duloxetine groups. In conclusion, duloxetine has no direct effect on tumor growth and does not alter immunity. The drug increased the SOD that fights free radicals and led the migration of lymphocytes, suggesting that duloxetine could be used in tumor-bearing individuals.

Antimalarial potential of leaves of Chenopodium ambrosioides L.

In an effort to identify novel therapeutic alternatives for the treatment of malaria, the present study evaluated the antimalarial effect of the crude hydroalcoholic extract (HCE) from the leaves of Chenopodium ambrosioides L. For this purpose, the molecular affinity between the total proteins from erythrocytes infected with Plasmodium falciparum and HCE or chloroquine was evaluated by surface plasmon resonance (SPR). Subsequently, the plasmodicidal potential of HCE was assessed in a P. falciparum culture. Using BALB/c mice infected with Plasmodium berghei intraperitoneally (ip.), we evaluated the effects of ip. treatment, for three consecutive days (day 7, 8, and 9 after infection), with chloroquine (45 mg/kg) or HCE (5 mg/kg), considering the survival index and the parasitaemia. The groups were compared to an untreated control group that receives only PBS at the same periods. The results indicated that HCE could bind to the total proteins of infected erythrocytes and could inhibit the parasite growth in vitro (IC50 = 25.4 g/mL). The in vivo therapeutic treatment with HCE increased the survival and decreased the parasitaemia in the infected animals. Therefore, the HCE treatment exhibited a significant antiplasmodial effect and may be considered as a potential candidate for the development of new antimalarial drugs.