Akademik Veri Yönetim Sistemi
19th International Congress of Immunology, Vienna, Avusturya, 17 - 22 Ağustos 2025, (Yayınlanmadı)
Introduction: Chronic lymphocytic
leukemia (CLL) is most common type of leukemia in Western countries and its
pathogenesis associated with the defect in apoptosis. Dioscin,
a typical saponin with multiple pharmacological activities, has also recently
been shown to induce apoptosis in many cancer cells. The
Node-like receptor protein 3 (NLRP3) inflammasome is a multimeric cytosolic
protein complex that is recruited in response to cellular disruptions. However,
dioscin has been shown to inhibit NLRP3
inflammasome.
Objectives: There is no study on
whether dioscin causes cell death and its effects on the expression of NLRP3,
ASC, caspase-1, IL-1β and IL-18 in CLL cells. Therefore, this study aims to examine the effects of dioscin on the
expression of NLRP3 inflammasome and apoptosis in CLL cell lines.
Methods: In this study, dioscin was treated to
PGA-1, CII, MEC-1 human CLL cell lines under cell culture conditions for 24, 48
and 72 hours. As a result of cell viability analyses, IC50 values
of the cells were determined. After the determined IC50
concentrations of dioscin were treated to the cells, the cells were stained
with annexin V-FITC and propidium iodide and apoptosis was determined by flow
cytometry. Protein expression levels were analyzed by flow cytometric analysis
by staining the cells with fluorescently labeled NLRP3, ASC, caspase-1, IL-1β
and IL-18 antibodies.
Results: Dioscin
induces apoptosis and reduces NLRP3, ASC, caspase-1, IL-1β and IL-18 protein
levels in all cell lines.
Conclusion: Dioscin might be a potential anti-cancer therapeutic for chronic lymphocytic
leukemia and therefore, determination of the
exact molecular effects of dioscin with future in vivo and in vitro studies
will enable the identification of new molecular targets for the treatment of
CLL.