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The current standard therapy of patients with chronic hepatitis C is the combination of peg‐interferon (IFN)‐α and ribavirin.However, it is well known that interferon in combination with ribavirin treatment may exacerbate the neutropenia and thrombocytopenia in those patients. Danazol therapy seems to be a useful and well‐tolerated treatment for refractory immune thrombocytopenic associated with several autoimmune diseases. The aim of this work was to investigate whether the simultaneous administration of peg‐interferon, ribavirin and danazol mofify the liver fibrosis. Male Wistar were included in: Control; Danazol (0.166mg/day); IFN (1.2μg/week) + Ribavirina (1 mg/day); IFN + Rib + Dan; CCl4 (0.4 g/kg/ 8 weeks); CCl4 + IFN + Rib; CCl4 + IFN + Rib + Dan. At the end of treatment we analyzed liver function and morphology, collagen content, and the mRNA for TGF‐beta1, TNF‐alpha, PDGF e interleukins (1, 6 and 10). Our results showed that the combined treatment with peg‐interferon, ribavirin and danazol improved the liver function and architecture. It was reduced the total amount of collagen which correlated with the collagen bands in liver tissue. The treatment with peg‐interferon, ribavirin and danazol induce a change in the patron of expression of pro‐imflamatory and anti‐inflamatory cytokines. Therefore the combine treatment with treatment with peg‐interferon, ribavirin and danazol appear to be a new terapeutic option in those patients with chronic hepatitis C virus infection.

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Globally breast cancer is the most common cancer in women. The chemotherapy treatment is successful in many instances, however, some patients do not respond satisfactorily. The multi‐drug resistance is considered the principal cause of failure of chemotherapy. There are different mechanisms by which originates multidrug resistance. It has been found that resistance is associated with ABC transporters, mainly P‐glycoprotein (P‐gp). Displayed can be modulated by compounds of natural origin, such as green tea and its polyphenols, including (−)‐Epigallocatechin‐3‐gallate (EGCG). The aim of this study is to observe the effect of EGCG on expression and activity of P‐glycoprotein in cell lines of breast cancer. We use the cell line MCF‐7. We evaluated the effect of EGCG on viability by MTT assay and fluorescence. Also we evaluated the effect on the expression of P‐gp by western blot and immunofluorescence. The activity was measured by the technique of Rhodamine123 accumulation. We found that EGCG does not cause cell death at concentrations below 100 μM. However, concentrations greater than 100 μM produces two types of cell death concentration dependent, EGCG 250 μM produces death by apoptosis and concentrations greater than 500 μM produces death by necrosis. EGCG decreases the expression and activity of Pg‐p in a dose dependent. We conclude that EGCG can reverse drug resistance associated with P‐gp in vitro assays.

Several plants have been used by their medical benefits. The responsible of these benefits are phytochemicals. Flavonoids have antioxidants, antifungal, antimicrobial proprieties and photoprotection activity. Gallic Acid is a phenolic acid that belong to the flavonoids group, this compound is abundant in strawberries, raspberries, black and green tea, and has been described antimicrobial and antifungal proprieties, as well as effects over drug metabolic enzymes. However, the mechanism of these effects has not been described. Membrane transporters have an important role in drug disposition. Since these flavonoids appear modify parameters such as absorption, distribution and metabolism of some drugs used in the treatment of some diseases, we analyze the effect of gallic acid over the expression of drugs transporters in hepatocytes. We treated HepG2 cells with different concentrations of gallic acid in order to establish the toxicological effects and the effect over proliferation of these cells by MTS assay, and then we observe the effect of the gallic acid over drugs transporters expression by inmunofluorescence detection. We observed that gallic acid has a toxicological effect in high concentrations and inhibits cell proliferation (0.1 and 1μM). However, gallic acid might induce the expression of drug transporters Pg‐P, OATP‐B and PEPT‐1 at low concentrations.

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