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Ewa Jaruga

Researcher at Nencki Institute of Experimental Biology

Publications -  6
Citations -  357

Ewa Jaruga is an academic researcher from Nencki Institute of Experimental Biology. The author has contributed to research in topics: Apoptosis & Curcumin. The author has an hindex of 5, co-authored 6 publications receiving 346 citations. Previous affiliations of Ewa Jaruga include University of Łódź.

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Journal ArticleDOI

Apoptosis-like, reversible changes in plasma membrane asymmetry and permeability, and transient modifications in mitochondrial membrane potential induced by curcumin in rat thymocytes

TL;DR: The sequence and extent of primary events induced by curcumin, in comparison with those occurring during dexamethasone‐induced apoptosis in rat thymocytes, are focused on and annexin VI‐FITC is presented as a new probe for studying membrane asymmetry.
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Effect of glutathione depletion on caspase-3 independent apoptosis pathway induced by curcumin in Jurkat cells.

TL;DR: Results show that in Jurkat cells curcumin prevents glutathione decrease, thus protecting cells against caspase-3 activation and oligonucleosomal DNA fragmentation, and induces nonclassical apoptosis via a still-unrecognized mechanism, which leads to chromatin degradation and high-molecular-weight DNA fragmentation.
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Apoptosis-independent alterations in membrane dynamics induced by curcumin.

TL;DR: This work chose the erythrocyte as a convenient model for studying membrane effects of curcumin and showed its nonspecific, apoptosis-independent way of action.
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Glutathione-independent mechanism of apoptosis inhibition by curcumin in rat thymocytes

TL;DR: Results show that CUR treatment elevated the concentrations of glutathione and nonprotein sulfhydryl groups, thus preventing their decrease in apoptotic thymocytes, suggesting a glutathionine-independent mechanism of cell protection.
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Proliferation and apoptosis of human T cells during replicative senescence--a critical approach.

TL;DR: A critical review of the polyclonal T cell replicative senescence model is presented and Immunoblotting analysis of p16 protein recognized previously as a marker of senescent T cells, showed its highest and transient expression in presenescent cells.