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Ellagic acid, a polyphenolic compound, selectively induces ROS-mediated apoptosis in cancerous B-lymphocytes of CLL patients by directly targeting mitochondria.

Salimi A, Roudkenar MH, Sadeghi L, Mohseni A, Seydi E, Pirahmadi N, Pourahmad J - Redox Biol (2015)

Bottom Line: Based on our results EA decreased the percentage of viable cells and induced apoptosis.EA increased ROS formation, mitochondria swelling, MMP decrease and cytochrome c release in mitochondria isolated from CLL BUT NOT healthy B-lymphocytes while pre-treatment with cyclosporine A and Butylated hydroxyl toluene (BHT) prevented these effects.Our results suggest that EA can act as an anti cancer candidate by directly and selectively targeting mitochondria could induce apoptosis through mitochondria pathway with increasing ROS production which finally ends in cytochrome c release, caspase 3 activation and apoptosis in cancerous B-lymphocytes isolated from CLL patients.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

No MeSH data available.


Related in: MedlinePlus

The effect of EA on ΔΨm of healthy and CLL B-lymphocytes (A and B). Freshly isolated purified B-lymphocytes were incubated with 25 µM EA for 24 h. ΔΨm was measured following rohodamine 123 staining with flow cytometry. The presented data revealed that exposure to EA caused a significant decrease in ΔΨm in CLL B-lymphocytes compared with those suspended in the EA-free medium with 0.05% (v/v) DMSO (untreated CLL control).
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f0025: The effect of EA on ΔΨm of healthy and CLL B-lymphocytes (A and B). Freshly isolated purified B-lymphocytes were incubated with 25 µM EA for 24 h. ΔΨm was measured following rohodamine 123 staining with flow cytometry. The presented data revealed that exposure to EA caused a significant decrease in ΔΨm in CLL B-lymphocytes compared with those suspended in the EA-free medium with 0.05% (v/v) DMSO (untreated CLL control).

Mentions: To search for the indication of mechanisms involved in apoptosis, we examined the effects of EA on ΔΨm. The treatment with EA (25 µM for 24 h) had higher percentage of low ΔΨm in CLL B-lymphocytes in comparison to the healthy B-lymphocytes (Fig. 5).The change of ΔΨm in CLL B-lymphocytes has been shown with arrow.


Ellagic acid, a polyphenolic compound, selectively induces ROS-mediated apoptosis in cancerous B-lymphocytes of CLL patients by directly targeting mitochondria.

Salimi A, Roudkenar MH, Sadeghi L, Mohseni A, Seydi E, Pirahmadi N, Pourahmad J - Redox Biol (2015)

The effect of EA on ΔΨm of healthy and CLL B-lymphocytes (A and B). Freshly isolated purified B-lymphocytes were incubated with 25 µM EA for 24 h. ΔΨm was measured following rohodamine 123 staining with flow cytometry. The presented data revealed that exposure to EA caused a significant decrease in ΔΨm in CLL B-lymphocytes compared with those suspended in the EA-free medium with 0.05% (v/v) DMSO (untreated CLL control).
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588415&req=5

f0025: The effect of EA on ΔΨm of healthy and CLL B-lymphocytes (A and B). Freshly isolated purified B-lymphocytes were incubated with 25 µM EA for 24 h. ΔΨm was measured following rohodamine 123 staining with flow cytometry. The presented data revealed that exposure to EA caused a significant decrease in ΔΨm in CLL B-lymphocytes compared with those suspended in the EA-free medium with 0.05% (v/v) DMSO (untreated CLL control).
Mentions: To search for the indication of mechanisms involved in apoptosis, we examined the effects of EA on ΔΨm. The treatment with EA (25 µM for 24 h) had higher percentage of low ΔΨm in CLL B-lymphocytes in comparison to the healthy B-lymphocytes (Fig. 5).The change of ΔΨm in CLL B-lymphocytes has been shown with arrow.

Bottom Line: Based on our results EA decreased the percentage of viable cells and induced apoptosis.EA increased ROS formation, mitochondria swelling, MMP decrease and cytochrome c release in mitochondria isolated from CLL BUT NOT healthy B-lymphocytes while pre-treatment with cyclosporine A and Butylated hydroxyl toluene (BHT) prevented these effects.Our results suggest that EA can act as an anti cancer candidate by directly and selectively targeting mitochondria could induce apoptosis through mitochondria pathway with increasing ROS production which finally ends in cytochrome c release, caspase 3 activation and apoptosis in cancerous B-lymphocytes isolated from CLL patients.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

No MeSH data available.


Related in: MedlinePlus