Curcumin/xanthan-galactomannan hydrogels: rheological analysis and biocompatibility.

Curcumin, a lipophilic compound found in the plant Curcuma longa L., exhibits a wide range of pharmacological activity; however, its therapeutic use has been limited because of its low bioavailability following oral administration. The aim of this study was to evaluate the viscoelastic characteristics and biocompatibility of a curcumin/xanthan:galactomannan hydrogel (X:G) system after topical application on chick embryo chorioallantoic membrane (CAM), a system established with a view toward curcumin nasal or topical pharmaceutical applications or possible administration in cosmetics or foods. A rheological analysis indicated that incorporation of curcumin did not alter the viscoelastic characteristics of the X:G hydrogel, suggesting that there was no change in the structure of the gel network. X:G hydrogels did not induce CAM tissue injury and the curcumin/X:G hydrogel system was also highly biocompatible. We conclude that the X:G hydrogel represents a potential matrix for curcumin formulations.

Calcarea carbonica e associações (M8) como tratamento adjuvante de carcinoma inflamatório mamário em cão / Calcarea carbonica derivative complex (M8) as adjuvant treatment of inflammatory mammary carcinoma in a dog

Background: Inflammatory mammary carcinoma (IMC) is locally aggressive, fast growing, highly malignant tumor that affects humans and dogs. Affected dogs usually are presented with generalized edema, pain, erythema, and skin ulceration in mammary glands. Surgery is not recommended and an effective treatment has not been established [1]. Calcarea carbonica derivative complex (M8) has demonstrated anticancer properties in a murine model, by improving innate immune response against tumor cells [2,3]. M8 is a complex high diluted medication comprised of a 10%-20% concentration of Calcarea carbonica, Aconitum napellus, Arsenicum album, Asa foetida, Conium maculatum, Ipecacuanha, Phosphorus, Rhus tox, Silicea, Sulphur, and Thuya occidentalis, all in decimal dilutions of Hahnemann in distilled water and submitted to vigorous shaking. Aim: Describe an association of M8 and piroxicam (Non-steroidal anti-inflammatory drug) to treat a dog with IMC. Discussion: A 7 years old, mixed breed intact female dog was presented to the Federal University of Parana - Veterinary Hospital, Curitiba (HV-UFPR) for mammary glands examination. The owners related inflammation of mammary glands with clinical course of approximately 10 days, which was treated for mastitis (cephalexin and metergoline) without clinical improvement. Clinical examination revealed erythema, increased skin warmth, pain on palpation, and plaque involving the 4th and 5th right mammary glands. Abdominal ultrasound and serum biochemistry were unremarkable. Thoracic radiographs showed suspicious images of pulmonary metastasis. Fine needle biopsy was taken for cytologic examination. Cytological interpretation was a malignant epithelial neoplasm, probably a mammary carcinoma. Diagnosis of IMC was based on clinical signs and cytopathology. Dog was treated with oral (0.5 mL) and topical M8 twice a day for 15 days, and pyroxican, 0.3mg/kg, PO, q24h. Clinical improvement was observed 7 days after starting treatment. Until present date (70 treatment days with M8), dog has no clinical signs of IMC, and does not show signs of disease progression. Conclusion: The present report suggests that M8 associated with piroxicam contributes to improvement of IMC dog?s quality of life and survival rate. However, further clinical studies are needed to evaluate response to treatment in patients diagnosed with IMC.(AU)

Introdução: O carcinoma inflamatório mamário (CIM) é um tumor altamente maligno que acomete cães e pessoas, apresentando-se localmente invasivo e com crescimento rápido. Em cães, os sinais clínicos incluem edema e eritema generalizado das mamas acometidas, dor local e ulceração. A intervenção cirúrgica é contra-indicada e não há consenso sobre tratamento clínico eficaz [1]. Estudos em modelo murino demonstraram que Calcarea carbonica e associações (M8) possuem propriedades anticancerígenas através de estímulo da resposta imune inata [2,3]. O M8 é altamente diluído, composto de 10 a 20% de Calcarea carbonica, Aconitum napellus, Arsenicum album, Asa foetida, Conium maculatum, Ipecacuanha, Phosphorus, Rhus tox, Silicea, Sulphur, e Thuya occidentalis, todos na diluição decimal de Hahnemann em água destilada e submetido à agitação vigorosa. Objetivo: Descrever a associação de M8 e piroxicam (antiinflamatório não esteroidal) no tratamento de cão com CIM. Discussão: Uma cadela não castrada, sem raça definida, de 7 anos de idade foi trazida ao Hospital Veterinário da Universidade Federal do Paraná - Curitiba (HV-UFPR) com histórico de inflamação mamária com evolução de 10 dias e não responsiva ao tratamento para mastite (com cefalexina e metergolina). Ao exame físico, as mamas abdominais caudais e inguinais direita apresentavam-se em placa, com aumento de temperatura, edema e eritema localizados e presença de sensibilidade dolorosa ao toque. A ultrassonografia abdominal e bioquímica sérica não apresentaram alterações significativas, enquanto que a radiografia torácica evidenciou imagem sugestiva de metástase pulmonar. Realizou-se biópsia aspirativa por agulha fina para análise citológica, a qual foi compatível com neoplasia epitelial maligna, provavelmente carcinoma mamário. O diagnóstico de CIM baseou-se nos sinais clínicos e resultados citopatológicos. Instituiu-se tratamento com M8 oral (0,5mL a cada 12 horas) e tópico (nas mamas envolvidas), em associação com piroxicam (0,3mg/kg, PO, a cada 24 horas). Observou-se melhora clínica significativa após 7 dias de tratamento e até a presente data (70 dias de tratamento com M8) a paciente não apresenta sinais clínicos de CIM e de progressão da doença.Conclusão: O presente caso sugere que a associação de M8 e piroxicam contribui para melhora da qualidade de vida e aumento da taxa de sobrevida em cães com CIM. No entanto, mais estudos são necessários para avaliar a resposta clínica de pacientes com CIM tratados com M8.(AU)

Avaliação da produção de citocinas pelos macrófagos J774. G8 após o tratamento com bioterápicos / Evaluation of cytokine production by J774. G8 macrophages after treatment with biotherapics

Strains of macrophages, such as murine J774.G8 macrophages, are susceptible to influenza A infection [1]. One of the responses to viral infection involves the production of various types of immunostimulatory cytokines by infected cells [2].In all cases, there were no significant differences compared to control groups. However, the production of TNF-? detected in macrophages treated by intact and inactivated biotherapics presented a tendency to increase after infection. In fact, similar results were previously detected in other experiments conducted only with the intact biotherapic [3]. The release of the cytokine MCP1 in all experimental situations presented a tendency to decrease after the viral infection when compared to untreated macrophages. No statistically significant difference was detected in the production of IL 12 and IL 10. These experiments will be repeated to confirm the data obtained.(AU)

Effects of citrinin on iron-redox cycle.

The ability of the mycotoxin citrinin to act as an inhibitor of iron-induced lipoperoxidation of biological membranes prompted us to determine whether it could act as an iron chelating agent, interfering with iron redox reactions or acting as a free radical scavenger. The addition of Fe3+ to citrinin rapidly produced a chromogen, indicating the formation of citrinin-Fe3+ complexes. An EPR study confirms that citrinin acts as a ligand of Fe3+, the complexation depending on the [Fe3+]:[citrinin] ratios. Effects of citrinin on the iron redox cycle were evaluated by oxygen consumption or the o-phenanthroline test. No effect on EDTA-Fe2+-->EDTA-Fe3+ oxidation was observed in the presence of citrinin, but the mycotoxin inhibited, in a dose-dependent manner, the oxidation of Fe2+ to Fe3+ by hydrogen peroxide. Reducing agents such as ascorbic acid and DTT reduced the Fe3+-citrinin complex, but DTT did not cause reduction of Fe3+-EDTA, indicating that the redox potentials of Fe3+-citrinin and Fe3+-EDTA are not the same. The Fe2+ formed from the reduction of Fe3+-citrinin by reducing agents was not rapidly reoxidized to Fe3+ by atmospheric oxygen. Citrinin has no radical scavenger ability as demonstrated by the absence of DPPH reduction. However, a reaction between citrinin and hydrogen peroxide was observed by UV spectrum changes of citrinin after incubation with hydrogen peroxide. It was also observed that citrinin did not induce direct or reductive mobilization of iron from ferritin. These results indicate that the protective effect on iron-induced lipid peroxidation by citrinin occurs due to the formation of a redox inactive Fe3+-citrinin complex, as well as from the reaction of citrinin and hydrogen peroxide.