Curcuma longa is able to induce apoptotic cell death of pterygium-derived human keratinocytes

Copyright © 2017 Silvia Sancilio et al. Pterygium is a relatively common eye disease that can display an aggressive clinical behaviour. To evaluate the in vitro effects of Curcuma longa on human pterygium-derived keratinocytes, specimens of pterygium from 20 patients undergoing pterygium surgical excision were collected. Pterygium explants were put into culture and derived keratinocytes were treated with an alcoholic extract of 1.3% Curcuma longa in 0.001% Benzalkonium Chloride for 3, 6, and 24 h. Cultured cells were examined for CAM5.2 (anti-cytokeratin antibody) and CD140 (anti-fibroblast transmembrane glycoprotein antibody) expression between 3th and 16th passage to assess cell homogeneity. TUNEL technique and Annexin-V/PI staining in flow cytometry were used to detect keratinocyte apoptosis. We showed that Curcuma longa exerts a proapoptotic effect on pterygium-derived keratinocytes already after 3 h treatment. Moreover, after 24 h treatment, Curcuma longa induces a significant increase in TUNEL as well as Annexin-V/PI positive cells in comparison to untreated samples. Our study confirms previous observations highlighting the expression, in pterygium keratinocytes, of nuclear VEGF and gives evidence for the first time to the expression of nuclear and cytoplasmic VEGF-R1. All in all, these findings suggest that Curcuma longa could have some therapeutic potential in the treatment and prevention of human pterygium

Evidence for an early and transient involvement of nuclear inositol lipids insubcellular signalling events related to DNA repair processes

The involvement of nuclear inositol lipids in the processes related to DNA repair upon ionizing radiation has been investigated in Murine Erythroleukaemia cells. Early changes in the in vitro phosphatidylinositol-bisphosphate phosphorylation in isolated nuclei were found to precede transiently the marked increase in DNA synthesis occurring after irradiation. Such an increase detected by anti-BrdU monoclonal antibodies has been found to be related mainly to DNA polymerase beta activity as revealed by the kinetic analysis of in vitro DNA synthesis. The results here presented allow us to speculate on a possible involvement of nuclear inositol lipids in the cascade of the early events leading to the regulation of DNA repair in the nucleus

Role of nuclear PKC delta in mediating caspase-3-upregulation in Jurkat T leukemic cells exposed to ionizing radiation.

The response of Jurkat T cells to ionizing radiation (IR) includes cell cycle arrest and DNA damage, which lead to the occurrence of apoptosis. Here, we try to elucidate some of the early intracellular signals which control the induction of such a process upon IR exposure, addressing to examine the specific role of several PKC isoforms (delta, epsilon, zeta) and their subcellular distribution. Attention has been focused on the connections between nuclear PKC delta activation and the expression of cell death regulators (Bcl-2 family proteins Bad, Bax and Bcl-2) and cell death effector caspase-3 (CPP32) which lead to the cleavage of cytoskeletal and nuclear proteins and induction of apoptosis. Altogether these results let us to conclude that PKC delta, potentiating the pro-apoptotic effect of caspase 3, plays a key role in the cellular response to IR and thus can be considered a molecular target for therapy

Clínquer Portland com reduzido impacto ambiental

Atualmente há um expressivo aumento no consumo de cimento, aliado à crescente preocupação ambiental inserida dentro do processo industrial. Com o intuito de amenizar impactos gerados pelo consumo de matéria-prima e emissão de CO2 para a atmosfera, foi realizado um estudo em laboratório no qual a escória do forno panela (EFP), um resíduo da indústria siderúrgica, foi empregada para fabricação do clínquer Portland. O objetivo é avaliar a qualidade do clínquer e a emissão de CO2 gerada ao adicionar esse subproduto na farinha do clínquer. Foram realizadas análises termogravimétricas para quantificar as emissões de CO2 por farinhas sem e com EFP, a partir da avaliação de sua decomposição em elevadas temperaturas. Os clínqueres produzidos foram avaliados qualitativamente por difração de raios X e microscopia óptica. Os resultados demonstram que o clínquer produzido com EFP tem uma emissão de CO2 16,51% mais baixa que o clínquer referência, produzido apenas com reagentes químicos puros. Os resultados dessa análise mineralógica por difração de raios X e microscopia óptica de luz refletida mostraram-se satisfatórios, observando-se uma melhor queimabilidade da farinha com EFP

Exercise training reduces fibrosis and matrix metalloproteinase dysregulation in the aging rat heart

Aging impairs function in the nonischemic heart and is associated with mechanical remodeling. This process includes accumulation of collagen (i.e., fibrosis) and dysregulation of active matrix metalloproteinases (MMPs). Exercise training (ET) improves cardiac function, but the pathways of protection remain poorly understood. Young (3 mo) and old (31 mo) FBNF1 rats were assigned into sedentary and exercise groups, with ET group rats training on a treadmill 45 min/d, 5 d/wk for 12 wk. Nonlinear optical microscopy (NLOM), histology, immunohistochemistry (IHC), and Western blot analyses were performed on the left ventricle and septum. NLOM, IHC, and histological imaging revealed that ET reduced age-associated elevation of collagen type I fibers. Active MMP-1, active MMP-2, and MMP-14 in the ECM fraction of the left ventricle were reduced by aging, an effect abrogated by ET. Tissue inhibitor of MMP (TIMP-1) was elevated with age but protected by ET. Transforming growth factor-β (TGF-β), upstream regulator of TIMP-1, increased with age but was attenuated by ET. Therefore, exercise training could protect the aging heart against dysregulation of MMPs and fibrosis by suppressing elevation of TIMP-1 and TGF-β.—Kwak, H.-B., Kim, J.-H., Joshi, K., Yeh, A., Martinez, D. A., Lawler, J. M. Exercise training reduces fibrosis and matrix metalloproteinase dysregulation in the aging rat heart