Anti-beta Galactosidase polyclonal antibody

Replicative capacity of somatic cells is limited. It indicates that aging also develops at the cellular level, and this is described as "cellular senescence". Senescent cells become flattened, enlarged, and irreversibly lose capacity for proliferation. Lack of specific and conclusive markers for cellular senescence makes it difficult to comprehensively define and understand this biological process especially in vivo. Molecules including p53, p21, p16(In)(k4)(a), p38MAPK, and gamma H2AX, telomere attrition, enhanced signals for SA-beta-gal, etc. are widely used to detect senescent cells, but these are indirect indicators of cellular senescence, and biological markers reflecting direct evidence need to be established. Genetic profiles are altered in senescent cells, letting these cells secrete pro-inflammatory molecules. Aging or age-related disorders including heart failure and atherosclerotic diseases link with an accumulation of cells undergoing cellular senescence in cardiovascular systems including heart and vessels. Senescent cells become pathogenic in most cases by mediating chronic sterile inflammation and tissue remodeling. A recent conceptual as well as technical breakthrough in this research area is "senolysis", meaning the specific elimination of senescent cells. Genetic as well as pharmacological models with senolysis contributed to reverse aging phenotypes and ameliorated pathologies in age-related disorders without enhancing the risk of tumorigenesis, and opened a new avenue for aging research. Several compounds are identified as senolytics, and some are already tested in clinical settings. It was recently reported that senolysis reverses aging phenotype in cardiovascular disorders. Generating therapies targeting suppression or elimination of senescent cells would inhibit the progression of undesirable aspects of aging, and become promising therapies for cardiac diseases. (C) 2019 The Authors. ISDN. Published by Elsevier Ltd.

Purpose: Pentagamavunon-1 (PGV-1) is a curcumin analogue that shows cytotoxic activity in various cancer cells. In this study, we evaluated the effect of PGV-1 on a highly metastatic breast cancer cell line, the 4T1 cells, as an anti-metastatic and anti-proliferative agent. Methods: Cell viability was evaluated using MTT assay; while cell cycle profile, apoptosis incidence, and ROS intracellular level were determined by flow cytometry. Cell senescence was observed under senescence-associated-beta-galactosidase (SA-beta-gal) staining assay. The expression of matrixmetalloproteinase-9 (MMP-9) was determined using immunoreaction based-ELISA, while other proteins expression were detected using immunoblotting. Results: Curcumin and PGV-1 showed cytotoxic effects on 4T1 cells with IC50 value of 50 and 4 mu M, respectively. The cytotoxic activity of PGV-1 was correlated to the induction of G2/M cell cycle arrest and cell senescence. Furthermore, PGV-1 increased the accumulation of intracellular ROS level. We also revealed that PGV-1 bound to several ROS-metabolizing enzymes, including glyoxalase I (GLO1), peroxiredoxin 1 (PRDX1), N-ribosyldihydronicoiinamide: quinone reductase 2 (NQO2), aldo-lceto reductase family 1 member c1 (AKR1C1). As an anti-metastatic agent, PGV-1 showed less inhibitory effect on cell migration compared to curcumin. However, PGV-1 significantly decreased MMP-9 protein expression in a dose-dependent manner suggesting it still potent to inhibit metastatic cells. Conclusion: Overall, our findings suggest that PGV-1 is potential to be developed as an anti-proliferative and anti-metastatic agent.