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.
At present there are not effective drugs for fungal infections. The amphotericin B has been used during 45 years. However, dose dependent nephrotoxicity has been a persistent problem, often limiting its administration in full therapeutic dosages. An alternative approach for limiting amphotericin nephrotoxicity has been to synthesize new analogous. The aim of this work was to evaluate and compare the toxicity of and analog of amphotericin B in BalB‐c mice. For the study we used male mice 25g whom received 4 mg/kg of analogous and amphotericin B by i.p., during 10 days in unique dosage every third day. After treatment animals were sacrificed and were analyzed the renal function and was done and histological and ultrastructural analysis of renal tissue, as well as was evaluated the effect on bone marrow. Our result showed an increase in the urea levels (37.5% y 33.5%) with amphotericin B and the analogue, respectively. The synthetic analogue showed morphological alterations in glomerules, renal tubules and mitochondries. As well as were observed the presence of some cells in apoptosis and necrosis. Animals treated with amphotericin B showed great amount of cell in apoptosis as well as membranal and mitochondrial alterations. Any compound induced changes in bone marrow. Our result showed that the synthetic analogue was less toxic than amphotericin B in mice.
Ethanol (EtOH) consumption is a well‐established risk factor for breast cancer in women. However, the mechanism by which EtOH exerts its carcinogenic activity in breast tissue remains known. In the present work, we analyze the ethanol metabolic enzymes in primary human mammary epithelial cells (HMEC) and MCF10A cells and to study the role of those enzymes in ethanol‐ induced oxidative stress and EGFR activation. Our results show that EtOH decreased CYP2E1 protein expression at 10, 30 and 100 mM when cells were treated every 12 h for 3 days. We also found that 30 and 100 mM EtOH increased ROS levels after 2 h treatment in CYP2E1over‐expressing 4.1.2E1 cells. Additionally, we found that in CYP2E1over‐expressing 4.1.2E1 cells increased the level of pY1086 EGFR phosphorylation after 18 h ethanol treatment. These studies suggest that ethanol can transactivate EGFR and activate downstream cell signaling in MCF10A cells, mediated by oxidative stress. These studies were supported in part by NIH RO1 ES‐07259 and by CONACYT ‐Mexico a Fellowship to Angel León‐Buitimea number 212849.
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