In vitro modulation of pancreatic min6 insulin secretion and proliferation and extrapancreatic glucose absorption by paronychia argentea, rheum ribes and teucrium polium extracts

The present study design investigated the effects of crude aqueous extracts [AE] of Paronychia argentea Lam., Rheum ribes L. and Teucrium polium L., traditionally utilized in diabetes treatment in Jordan, on the pancreatic beta-cell MIN6 proliferation and insulin secretion and extrapancreatic glucose diffusion. In an ascending order, R. ribes, T. polium and P. argentea concentrations induced a MIN6 monolayers expansion by respective 118-136%, 158-175% and 140-200% [P<0.001], thus exceeding GLP-1 [5 nM] pancreatic proliferative capacity. Like Lalanine [10 mM] insulinotropic efficacy and without exerting cytotoxicity, glucose stimulated insulin secretion was potentiated by AEs of R. ribes [373-736%, P<0.001] and T. polium [503-1190% P<0.001]. P. argentea AE was inactive at used doses. The potent plants' insulin secretory bioactivities were abolished in the depleted Ca[2+] conditions [P<0.001]. Comparable to guar gum [50 mg/ml] diffusional hindrance in a simple dialysis model, P. argentea inhibited overnight glucose movement in vitro [by 38.1 +/- 1.9% AUC reductions, P<0.001], while R. ribes and T. polium AEs proved inactive. This in vitro evaluation has revealed that all three plants augmented beta- cell expansion, P. argentea inhibited carbohydrate absorption and R. ribes and T. polium stimulated insulin secretion. These actions depend on their intact absorption in vivo. Future directives may assess the use of P. argentea, R. ribes and T. polium as new potential sources with functional properties for food or nutraceutical products or active leads into anti-diabetes pharmacotherapy

Some insights into the cellular responses against doxorubicin and actinomycin D

Cellular responses to anti-cancer agents are an important factor in recognizing mechanisms of resistance and in identifying new treatment biomarkers. In this study, we have compared the effect of actinomycin D and doxorubicin on selected genes in the transcription and ubiquitin pathways. The human promyelocytic leukemia cells [HL60] was used as a model system and the chosen genes were POL2A and ELL2 [from transcription machinery] and UBE2DE and CDC [from ubiquitin pathway]. The responses of the four targeted genes suggested a degree of biological resistance amongst just those functions that might be expected to be damaged by the drug action. It is as if the cells are trying to upregulate these functions to offset drug inhibition. For example, doxorubicin up-regulated ubiquitinrelated genes suggesting an attempt to remove the trapped cleavable complex by an ubiquitin-dependent mechanism, while actinomycin up-regulated the transcription machinery genes suggesting an attempt to overcome the longed lived complexes that are formed by the actinomycin D on the DNA