Search

Objectives Gymnema montanum Hook, an Indian Ayurvedic medicinal plant, is used traditionally to treat a variety of ailments. Here, we report anti-cancer effects and molecular mechanisms of ethanolic extract of G. montanum ( GLEt) on human leukaemia HL-60 cells, compared to peripheral blood mononuclear cells. Materials and methods HL-60 cells were treated with different concentrations of GLEt (10-50 μg/ml) and cytotoxicity was assessed by MTT assay. Levels of lipid peroxidation, antioxidants, mitochondrial membrane potential and caspase-3 were measured. Further, apoptosis was studied using annexin-V staining and the cell cycle was analyzed by flow cytometry. Results GLEt had a potent cytotoxic effect on HL-60 cells ( IC50-20 μg/ml), yet was not toxic to normal peripheral blood mononuclear cells. Exposure of HL-60 cells to GLEt led to elevated levels of malonaldehyde formation, but to reduced glutathione, superoxide dismutase, catalase and glutathione peroxidase activities ( P < 0.05). Induction of apoptosis was confirmed by observing annexin-V positive cells, associated with loss of mitochondrial membrane potential. Cell cycle arrest at G0/G1 was observed in GLEt-treated HL-60 cells, indicating its potential at inducing their apoptosis. Conclusions Findings of the present study suggest that G. montanum induced apoptosis in the human leukaemic cancer cells, mediated by collapse of mitochondrial membrane potential, generation of reactive oxygen species and depletion of intracellular antioxidant potential. [ABSTRACT FROM AUTHOR]

Analyzes the cell-free filtrates from high-density Chlorella vulgaris (Chlorellaceae) for the presence of any inhibitory /cell cycle inhibitory compounds. Effect of conditioned medium; Characterization of factors responsible for cell cycle modulation; Effect of bicarbonate concentration; Effect of bicarbonate-free conditioned medium.

Objective Endothelial dysfunction highlights that it is a potential contributor in the pathogenesis of vascular complications arising from endoplasmic reticulum stress ( ER stress) and has been emerging as a main causative factor in vascular failure. Here, we hypothesize that the natural flavonoid, quercetin plays an effective role in reducing ER stress in human umbilical vein endothelial cells. Materials and methods Human umbilical vein endothelial cells were pre-treated with different concentrations of quercetin (0-100 μ m) before inducing ER stress using tunicamycin ( TUN) (0.75 μg/ml); cytotoxicity was assessed by MTT assay. Expression levels of ER stress responsive genes, antioxidant enzymes and apoptotic markers were assessed by qRT- PCR, while roles of caspase-3 and PARP cleavage were measured by western blot analysis. Results Quercetin pre-treatment at 25 and 50 μ m had a cytoprotective effect on cells against TUN-induced toxicity. Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 ( GRP78) and C/EBP-homologous protein ( CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay. Induction of apoptosis was prevented with reduction in expression level of Bax, and concomitant increase in Bcl-2 levels, thus proving its potential against ER stress. Conclusion The current study indicates that quercetin modulated stress responsive genes GRP78 and CHOP, helping endothelial cells prevent TUN-induced ER stress. [ABSTRACT FROM AUTHOR]