Efeito da curcumina, um inibidor do fator de transcrição NFkB, sobre a viabilidade de neuroblastoma SH-SY5Y humano diferenciado e indiferenciado, quando desafiado por peróxido de hidrogênio

Introdução: A curcumina mostrou uma capacidade significativa de diminuir muitas das características de câncer. Além disso, o fator de transcrição nuclear NF-κB é um importante complexo das reações inflamatórias das células e está envolvido em vários tipos de crescimento canceroso. Também, o peróxido de hidrogênio mostrou a capacidade a ativar o fator de transcrição de NF-κB. Assim, a possibilidade de utilizar as características anti-inflamatórias da curcumina para inibir a ativação do NF-κB existe. Resultados: Nós encontramos que nas concentrações mais altas da curcumina utilizadas no experimento, tanto sozinha quanto em cotratamento com o H2O2, houve uma redução na viabilidade na SH-SY5Y indiferenciada. Contudo, também encontramos que a curcumina sozinha reduziu a viabilidade na SH-SY5Y diferenciada nas concentrações mais altas depois da incubação de 24h. Nós podemos deduzir que os efeitos da curcumina na SH-SY5Y são devidos à inibição citosólica da via do NF-κB uma vez que reduz a translocação de p65. Conclusão: As evidências apontam para a funcionalidade relativa da curcumina a inibir a ativação de NF-κB nas concentrações mais altas.Introduction: Curcumin has shown a significant ability to reduce many of the characteristics of cancer. Moreover, the nuclear transcription factor NF-κB is an important complex of inflammatory reactions in cells, and is implicated in several types of cancerous growth as well. Also, hydrogen peroxide has shown the ability to activate the transcription factor NF-κB. Thus, the possibility of using the anti-inflammatory characteristics of curcumin to inhibit activation of NF-κB exists. Results: We found that higher concentrations of curcumin, both alone and in cotreatment with H2O2, induced a decrease in viability in undifferentiated SH-SY5Y. However, we also found that curcumin alone reduced the viability in differentiated SH-SY5Y at the higher concentrations of curcumin after incubation for 24h. We can deduce the effects of curcumin on SH-SY5Y are due to the inhibition of the cytosolic pathway of NF-κB, since it reduces the translocation of p65. Conclusion: The evidence points to the functionality of curcumin to inhibit NF-κB in the highest concentrations

HAND770212_Appendix – Supplemental material for A Survey of Fellowship-Trained Upper Extremity Surgeons on Treatment of Lateral Epicondylitis

<p>Supplemental material, HAND770212_Appendix for A Survey of Fellowship-Trained Upper Extremity Surgeons on Treatment of Lateral Epicondylitis by Steven R. Niedermeier, Nisha Crouser, Amy Speeckaert and Kanu S. Goyal in HAND</p

Pivotal role of CD4(+) T cells in renal fibrosis following ureteric obstruction

Tubulointerstitial fibrosis is a common consequence of a diverse range of kidney diseases that lead to end-stage renal failure. The degree of fibrosis is related to leukocyte infiltration. Here, we determined the role of different T cell populations on renal fibrosis in the well-characterized mouse model of unilateral ureteric obstruction. Depletion of CD4+ T cells in wild-type mice with a monoclonal antibody significantly reduced the amount of interstitial expansion and collagen deposition after 2 weeks of obstruction. Reconstitution of lymphopenic RAG knockout mice with purified CD4+ but not CD8+ T cells, prior to ureteric obstruction, resulted in a significant increase in interstitial expansion and collagen deposition. Wild-type mice had significantly greater interstitial expansion and collagen deposition compared with lymphopenic RAG−/− mice, following ureteric obstruction; however, macrophage infiltration was equivalent in all groups. Thus, our results suggest that renal injury with subsequent fibrosis is likely to be a multifactorial process, with different arms of the immune system involved at different stages. In this ureteric obstruction model, we found a critical role for CD4+ T cells in kidney fibrosis. These cells could be a potential target of therapeutic intervention to prevent excessive fibrosis and loss of function due to renal injury