مقالات پذیرفته شده کنگره

  • Immunohistochemical Analysis of Apoptosis (p53/Bax) and Autophagy Markers in Glioblastoma Pathomorphosis Induced by Non-Invasive Phototherapy

  • Alexander Shirokov,1 Arina Evsyukova,2 Mohammad Reza Rashidian Vaziri,3 Armin Imanparast,4 Ameneh Sazgarnia,5,* Samaneh Sharif,6
    1. Saratov State University, Astrakhanskaya Str., 83, Saratov 410012, Russia & Institute of Biochemistry and Physiology of Plants and Microorganisms, Saratov Scientific Centre of the Russian Academy
    2. Saratov State University, Astrakhanskaya Str., 83, Saratov 410012, Russia
    3. Department of Physics, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
    4. Medical Physics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran & Department of Medical Physics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
    5. Medical Physics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran & Department of Medical Physics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
    6. Medical Genetics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran & Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran


  • Introduction: Evaluating the therapeutic pathomorphosis of glioblastoma (GB) through molecular and immunohistochemical (IHC) markers is crucial for understanding treatment efficacy. This study investigates the in vivo molecular mechanisms and pathomorphosis of transplanted C6 glioma in rats subjected to 1267 nm non-invasive laser therapy (LT).
  • Methods: The study included Wistar rats with implanted C6 glioblastoma, treated with daily LT sessions ($12.6~kJ/cm^2$) over three weeks. The molecular response was evaluated by analyzing IHC markers for apoptosis (p53, Bax, Fas-receptor), cellular proliferation (Ki-67), and autophagolysosome formation (LC3b, clathrin, caveolin).
  • Results: The in vivo application of LT increased the survival rate of the animal models from 34% to 64%. IHC analysis revealed a profound molecular shift in the tumor tissue: cellular proliferation was significantly suppressed, evidenced by a 1.6-fold decrease in Ki-67 expression. Furthermore, the treatment potently activated the mitochondrial apoptosis pathway, demonstrating a 13.5-fold increase in Bax protein expression and significant activation of the p53 protein. Concurrently, markers of autophagolysosome formation (LC3b, clathrin, and caveolin) were markedly inhibited.
  • Conclusion: The targeted therapy induces pronounced pathomorphosis in glioblastoma by shifting the molecular balance—downregulating proliferation and autophagy markers (Ki-67, LC3b) while upregulating crucial apoptotic pathways (p53, Bax). Assessing these molecular biomarkers provides deep insights into the efficacy of non-invasive therapies for aggressive brain tumors.
  • Keywords: Glioblastoma, Therapeutic Pathomorphosis, Apoptosis, Autophagy, Immunohistochemistry

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