В работе описаны результаты изучения функциональной морфологии саркомы М-1 крыс после фотодинамической терапии с применением в качестве фотосенсибилизатора дисульфидного производного бактериопурпуринимида (дисульфид-БПИ). Методы исследования включали иммуноокрашивание на PCNA и CD31, определение митотической активности и апоптотической гибели опухолевых клеток, а также компьютерный анализ микроскопических изображений. Показано, что фотоиндуцированное противоопухолевое действие обусловлено разрушением сосудистого русла саркомы М-1, быстрым ингибированием пролиферативной активности и девитализацией опухолевых клеток путем апоптоза и некроза. Есть основания полагать, что в ранние сроки после фотодинамической терапии деструкция микроциркуляторного русла и фотоцитостатический шок опухолевых клеток с последующим развитием некроза обусловлены прямым воздействием светового потока на сенсибилизированные клеточные элементы паренхимы и стромы опухолей. Эффективность фотодинамической терапии с новым фотосенсибилизатором определяется последовательностью деструктивных и воспалительных изменений в паренхиме опухолей и окружающих тканях, а также репопуляционным потенциалом выживших после лечения опухолевых клеток.

Stroke remains the second leading cause of death worldwide. The development of new therapeutic agents focused on restoring vascular function and neuroprotection of viable tissues is required. In this study the neuroprotective activity of melanocortin-like ACTH(4–7)PGP and ACTH(6–9)PGP peptides was investigated in rat brain at 24 h after transient middle cerebral artery occlusion (tMCAO). The severity of ischemic damage, changes in the proliferative activity of neuroglial cells and vascularization of rat brain tissue were analyzed. The administration of peptides resulted in a significant increase in the volume density of neurons in the perifocal zone of infarction compared to rats subjected to ischemia and receiving saline. Immunohistochemical analysis of the proliferative activity of neuroglia cells using PCNA antibodies showed a significant increase in the number of proliferating cells in the penumbra and in the intact cerebral cortex of rats receiving peptide treatment. The effect of peptides on vascularization was examined using CD31 antibodies under tMCAO conditions, revealing a significant increase in the volume density of vessels and their sizes in the penumbra after administration of ACTH(4–7)PGP and ACTH(6–9)PGP. These findings confirm the neuroprotective effect of peptides due to the activation of neuroglia proliferation and the enhancement of collateral blood flow.

Ischemic stroke is a multifactorial disease that leads to brain tissue damage and severe neurological deficit. Transient middle cerebral artery occlusion (tMCAO) models are actively used for the molecular, genetic study of stroke. Previously, using high-throughput RNA sequencing (RNA-Seq), we revealed 3774 differentially expressed genes (DEGs) in the penumbra-associated region of the frontal cortex (FC) of rats 24 h after applying the tMCAO model. Here, we studied the gene expression pattern in the striatum that contained an ischemic focus. Striatum samples were obtained from the same rats from which we previously obtained FC samples. Therefore, we compared DEG profiles between two rat brain tissues 24 h after tMCAO. Tissues were selected based on magnetic resonance imaging (MRI) and histological examination (HE) data. As a result, 4409 DEGs were identified 24 h after tMCAO in striatum. Among them, 2609 DEGs were overlapped in the striatum and FC, whereas more than one thousand DEGs were specific for each studied tissue. Furthermore, 54 DEGs exhibited opposite changes at the mRNA level in the two brain tissues after tMCAO. Thus, the spatial regulation of the ischemic process in the ipsilateral hemisphere of rat brain at the transcriptome level was revealed. We believe that the targeted adjustment of the genome responses identified can be the key for the induction of regeneration processes in brain cells after stroke.