Optimal dose for photosensitizers-free PDT of glioma
Aleksandr Khorovodov, Saratov State University, Russia; Inna Blokhina, Saratov State University, Russia; Nikita Lezhnev, Saratov State University, Russia; Nikita Navolokin, Saratov State Medical University, Russia; Alexander Shirokov, Institute of Bioorganic Chemistry, Russian Academy of Sciences, Russia; Andrey Terskov, Saratov State University, Russia; Aysel Mamedova, Saratov State University, Russia; Aryna Evsukova, Saratov State University, Russia; Maria Klimova, Saratov State University, Russia; Ilana Agranovich, Saratov State University, Russia; Oxana Semyachkina-Glushkovskaya, Saratov State University, Russia
Abstract
Treatment of glioma is one of the most difficult tasks in neurooncology.
Photodynamic therapy (PDT) is a relatively new method in which photosensitizers (PSs)
selectively accumulate in tumors and, when exposed to laser radiation, generate singlet
oxygen(SO) which has a toxic effect on tumor. However, PSs have low specificity for
cancer cells. Due to the disappointing statistics on glioma control, there is great interest
in the development of PDT without the use of PSs. In this regard, we set the task to
determines the effective laser dose of quantum-dot 1268 nm laser which will suppress
the processes leading to the development of a tumor
We have demonstated that the 4 weeks course of PDT-357 J/cm2 causes
effective supression of glioma volume (decreased 1.5 times compared with the control
group without PDT(CG)) and an increase in the survival rate(increased 1.8 times vs.
CG) via stimulation of apoptosis(increased of apoptosis marker Bax 5 times vs. CG),
prevention of autophagy(decreased the Lc3s-immunopositive glioma cells 2.4 times vs.
CG ) and proliferation of cancer cells(decreased the proliferation marker Ki67 1.5 times
vs. CG.)
These results have show new strategy the supression of glioma growth and an
increase in the survival rate that were associated with a PDT-mediated prevention of
protective autophagy and high prolifiration of glioma cells with inducing of apoptotic cell
This work was supported by grants: RBRF 20-015-00308_а, RBF — 20-15-
00090, RF Goverment Grant 075-15-2019-1885.
Speaker
Aleksandr Khorovodov (khorovodov2012@yandex.ru)
Saratov State University
Russia
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