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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

Effects of EA on CLL and healthy B lymphocytes. EA-induced ROS generation in CLL but not in healthy B-lymphocytes (A and B). Changes mean of fluorescence intensity in ROS generation in CLL and healthy B-lymphocytes treated with EA 25 µM for 0–24 h summarized in graph D. Values (mean±S.E.) are from three independent experiments (D). *p<0.05, **p<0.01 for difference in ROS generation between healthy and CLL in time interval (D).
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f0020: Effects of EA on CLL and healthy B lymphocytes. EA-induced ROS generation in CLL but not in healthy B-lymphocytes (A and B). Changes mean of fluorescence intensity in ROS generation in CLL and healthy B-lymphocytes treated with EA 25 µM for 0–24 h summarized in graph D. Values (mean±S.E.) are from three independent experiments (D). *p<0.05, **p<0.01 for difference in ROS generation between healthy and CLL in time interval (D).

Mentions: In our study, EA treatment caused a significant increase in intracellular ROS levels in CLL B-lymphocytes (Fig. 4B) BUT NOT in healthy B-lymphocytes (Fig. 4A). In CLL B-lymphocytes, EA induced increase in intracellular ROS, which was not induced in healthy B-lymphocytes.


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)

Effects of EA on CLL and healthy B lymphocytes. EA-induced ROS generation in CLL but not in healthy B-lymphocytes (A and B). Changes mean of fluorescence intensity in ROS generation in CLL and healthy B-lymphocytes treated with EA 25 µM for 0–24 h summarized in graph D. Values (mean±S.E.) are from three independent experiments (D). *p<0.05, **p<0.01 for difference in ROS generation between healthy and CLL in time interval (D).
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0020: Effects of EA on CLL and healthy B lymphocytes. EA-induced ROS generation in CLL but not in healthy B-lymphocytes (A and B). Changes mean of fluorescence intensity in ROS generation in CLL and healthy B-lymphocytes treated with EA 25 µM for 0–24 h summarized in graph D. Values (mean±S.E.) are from three independent experiments (D). *p<0.05, **p<0.01 for difference in ROS generation between healthy and CLL in time interval (D).
Mentions: In our study, EA treatment caused a significant increase in intracellular ROS levels in CLL B-lymphocytes (Fig. 4B) BUT NOT in healthy B-lymphocytes (Fig. 4A). In CLL B-lymphocytes, EA induced increase in intracellular ROS, which was not induced in healthy B-lymphocytes.

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