Anti-E. coli Beta Galactosidase Polyclonal antibody

Purpose The aim of this study was to investigate the effects and possible mechanism of tea polyphenols (TPs) on the senescence of human glomerular mesangial cells (HGMCs) under high glucose conditions. Methods HGMCs were divided into the normal group (NG, 5.5 mmol/L glucose), mannitol group (MNT, 5.5 mmol/L glucose and 24.5 mmol/L mannitol), TP group (TP, 30 mmol/L glucose and 5 mu g/mL TP) and high-dose D-glucose group (HG, 30 mmol/L glucose). The effects of TP on the cell morphology of HGMCs; the percentage of cells positive for senescence-associated beta-galactosidase (SA-beta-gal); the ratio of G1 phase of cell cycle; telomere length; and the expression of p-Akt, p53, p21 and Rb proteins of the Akt-p53-p21 signaling pathway and the expression miR-126 were examined. Results High glucose led to premature senescence of HGMCs, as evident from the increase in the percentage of SA-beta-gal-positive cells, decrease in telomere length, cell cycle arrest at G1 phase,decrease in the expression of miR-126 and p-Akt and increase in the expression of p53, p21 and Rb proteins in the HG group. In contrast, in the TP group, these effects of high glucose treatment were abrogated and this indicates that TP had a protective effect on HGMCs. Conclusions High glucose induces the senescence of HGMCs in vitro via the miR-126 and Akt-p53-p21 signaling pathways. TP can delay the high glucose-induced senescence of HGMCs by regulating the activity of these signaling pathways. Thus, the polyphenols present in tea may have potential for the treatment of diabetic nephropathies associated with premature senescence.

Objectives Ageing is a universal and gradual process of organ deterioration. Radiation induces oxidative stress in cells, which leads to genetic damage and affects cell growth, differentiation and senescence. Astragaloside (AS)-IV has antioxidative, anti-apoptotic and anti-inflammatory properties. Methods To study the protective mechanism of AS-IV on radiation-induced brain cell senescence, we constructed a radiation-induced brain cell ageing model, using biochemical indicators, senescence-associated galactosidase (SA-beta-gal) senescence staining, flow cytometry and Western blotting to analyse the AS-IV resistance mechanism to radiation-induced brain cell senescence. Key findings Radiation reduced superoxide dismutase (SOD) activity and expressions of cyclin-dependent kinase (CDK2), CDK4, cyclin E and transcription factor E2F1 proteins, and increased expressions of p21, p16, cyclin D and retinoblastoma (RB) proteins, malondialdehyde (MDA) activity, SA-beta-gal-positive cells and cells stagnating in G1 phase. After treatment with AS-IV, the level of oxidative stress in cells significantly decreased and expression of proteins related to the cell cycle and ageing significantly changed. In addition, SA-beta-gal-positive cells and cells arrested in G1 phase were significantly reduced. Conclusions These data suggest that AS-IV can antagonize radiation-induced brain cells senescence; and its mechanism may be related to p53-p21 and p16-RB signalling pathways of ageing regulation.