20(S)-Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are members of the protopanaxadiol family and have been investigated for possible chemopreventive activity. This study explored the biological and apoptotic mechanisms induced by 20(S)-GRh2 in human acute leukaemia line-Reh cells. Reh cells were treated with different concentration of 20(S)-GRh2 in vitro. Cell viability was determined by Cell Counting Kit-8 and Annexin V/7-AAD assays. Mitochondrial membrane potential (MMP) was examined through JC-1 staining. Activation of caspases associated with the mitochondria-mediated apoptosis pathway was determined by Western blot. We observed that survival of Reh cells decreased after exposure to 20(S)-GRh2 in a concentration-dependent manner. Moreover, 20(S)-GRh2 can induce mitochondria depolarization of Reh cells as evident in the shift in JC-1 fluorescence from red to green. In addition, 20(S)-GRh2 induced the release of mitochondrial cytochrome c and activation of caspase-9 and caspase-3 in Reh cells. These results indicate that 20(S)-GRh2 could induce apoptosis through the mitochondrial pathway, demonstrating its potential as a chemotherapeutic agent for leukaemia therapy.

Download full-text PDF

Source
http://dx.doi.org/10.1248/bpb.b13-00667DOI Listing

Publication Analysis

Top Keywords

reh cells
20
20s-ginsenoside rh2
8
20s-grh2 induce
8
cells
6
20s-grh2
6
reh
5
rh2 induces
4
induces apoptosis
4
apoptosis human
4
human leukaemia
4

Similar Publications

This study investigates the interrelationship between human telomerase reverse transcriptase (hTERT) and ferroptosis in precursor-B (pre-B) acute lymphoblastic leukemia (ALL), specifically examining how hTERT modulation affects ferroptotic cell death pathways. Given that hTERT overexpression characterizes various cancer phenotypes and elevated telomerase activity is observed in early-stage and relapsed ALL, we investigated the molecular mechanisms linking hTERT regulation and ferroptosis in leukemia cells. The experimental design employed Nalm-6 and REH cell lines under three distinct conditions: curcumin treatment, hTERT siRNA knockdown, and their combination.

View Article and Find Full Text PDF

Retinal diseases often lead to degeneration of specific retinal cell types with currently limited therapeutic options to replace the lost neurons. Previous studies have reported that overexpression of or combinations of proneural factors in Müller glia (MG) induce regeneration of functional neurons in the adult mouse retina. Recently, we applied the same strategy in dissociated cultures of fetal human MG and although we stimulated neurogenesis from MG, our effect in 2D cultures was modest and our analysis of newborn neurons was limited.

View Article and Find Full Text PDF

Retinal degeneration in mammals causes permanent loss of vision, due to an inability to regenerate naturally. Some non-mammalian vertebrates show robust regeneration, via Muller glia (MG). We have recently made significant progress in stimulating adult mouse MG to regenerate functional neurons by transgenic expression of the proneural transcription factor Ascl1.

View Article and Find Full Text PDF
Article Synopsis
  • L-asparaginases are enzymes that convert L-asparagine into L-aspartic acid and ammonia, and they are important in the pharmaceutical industry, particularly for cancer treatments.
  • Scientists are exploring yeast-derived L-asparaginases as an alternative to bacterial ones, which can cause adverse immune responses.
  • The study focuses on a specific yeast enzyme, Lachancea thermotolerans, demonstrating that a mutant form of this enzyme shows increased activity and significant antileukemic potential compared to commercial bacterial versions.
View Article and Find Full Text PDF
Article Synopsis
  • Endogenous reprogramming of glial cells, specifically Müller glia, shows potential for neuron restoration in the adult retina by using strategies adapted from regenerative species.
  • The transcription factor Ascl1 can induce some Müller glia to regenerate neurons, but this process is hindered by neuroinflammation from infiltrating monocytes from the peripheral immune system.
  • Preventing monocyte infiltration enhances the neurogenic capacity of Müller glia, suggesting that targeting peripheral immune responses could improve neuronal regeneration therapies in the central nervous system.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!