Жарияланымдар / Публикации

Постоянный URI для этого сообществаhttps://cris.qyzpu.edu.kz/handle/123456789/2

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2025 - 20262

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Автор: search.filters.author.Lyailya BaktybayevaТема: search.filters.subject.hematopoietic recovery

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    Design, Characterization, and Hematopoietic Efficacy of a Fluorinated Pyrazolopiperidine Inclusion Complex
    (Multidisciplinary Digital Publishing Institute, 2025-10-11)
    Zhanargul Koshetova
    ;
    Guldana Daulet
    ;
    Assel Yu. Ten
    ;
    Raushan B. Koizhaiganova
    ;
    Lyailya Baktybayeva
    A novel inclusion complex of a fluorinated pyrazolopiperidine derivative (5-benzyl-7-(2-fluorobenzylidene)-2,3-bis(2-fluorophenyl)-3,3a,4,5,6,7-hexahydro-2H-pyrazolo [4,3-c]pyridine hydrochloride, PP·HCl) with β-cyclodextrin (PPβCD) was designed, synthesized, and characterized as a potential therapeutic agent for chemotherapy-induced myelosuppression and lymphopenia. Encapsulation of PP within β-cyclodextrin increased aqueous solubility by approximately 3.4-fold and improved dissolution rate by 2.8-fold compared with the free compound. Structural analysis using IR, ^1H/^13C NMR, and TLC confirmed the formation of a stable 1:1 host–guest complex, and the disappearance of free PP signals further supported complete encapsulation. In vivo evaluation in a cyclophosphamide-induced myelosuppression model demonstrated that PPβCD accelerated hematopoietic recovery, restoring leukocyte and erythrocyte counts 35–40% faster than methyluracil, without any signs of systemic toxicity. These findings indicate that β-cyclodextrin complexation significantly enhances solubility, dissolution, and biological efficacy of the pyrazolopiperidine scaffold, supporting further preclinical development of PPβCD as a supportive therapy for chemotherapy-related hematological complications.
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    Hematopoietic and T-lymphopoiesis-stimulating effects of a fluorinated pyrazolopiperidine β-cyclodextrin complex in cyclophosphamide-induced hematopoietic suppression
    (Frontiers Media, 2026-08-03)
    Assel Yu. Ten
    ;
    Lyailya Baktybayeva
    ;
    Zhanargul Koshetova
    ;
    Raushan B. Koizhaiganova
    ;
    Guldana Daulet
    Background Cyclophosphamide is widely used in oncology, autoimmune disorders, and transplantation-related conditioning or post-transplant immunosuppression. However, its therapeutic value is limited by hematopoietic and lymphoid toxicity, including leukopenia, neutropenia, anemia, thrombocytopenia, bone marrow suppression, thymic injury, and prolonged impairment of T-cell recovery. These effects may occur after pulsed intravenous administration, high-dose regimens used in transplantation or severe refractory disease, and continuous low-dose/metronomic exposure. Therefore, there is a medical need for pharmacological agents capable of compensating cyclophosphamide-induced hematopoietic and lymphopoietic suppression without causing uncontrolled stimulation of early progenitor cells. Aim To evaluate the hematopoietic and T-lymphopoiesis-stimulating activity of BIV under cyclophosphamide-induced hematopoietic and T-lymphopoietic suppression. Methods Cyclophosphamide-induced hematopoietic- and T-lymphopoiesis-suppressive models were established on laboratory albinos rats and C57BL6/J mice. Peripheral blood hematological indices in rats were measured using hematology analyzers. Hematopoietic stem cells, thymocyte subsets, Th act , T reg , T mem , CTL cell populations, and erythroid cells from the bone marrow, thymus, and spleen were analyzed by flow cytometry. Statistical analysis was performed using one-way ANOVA (p < 0.05). Results In rats with CPh-induced hematopoietic suppression, BIV supported partial recovery of erythrocyte and hemoglobin parameters and improved leukopoietic indices under CPh-induced hematopoietic suppression. The β-cyclodextrin complex of 5-benzyl-7-(o-fluorobenzylidene)-2,3-bis(o-fluorophenyl)-3,3a,4,5,6, 7-hexahydro-2H-pyrazolo[4,3-c]pyridine (BIV) demonstrated a consistent moderate activity in restoring the overall level of CD3ε+CD19− T lymphocytes in the bone marrow and thymus. In the bone marrow, BIV uniformly increased the reduced levels of CD3ε+CD19− T lymphocytes and CD3ε+CD44 + T mem memory T cells to physiological normal values. In the spleen, BIV restored the decreased levels of CD25+FoxP3+ T reg regulatory lymphocytes and CD28 + CD44 + T mem memory T cells to physiological normal levels, while reducing the elevated levels of CD3ε+CD8a+ CTL cytotoxic T lymphocytes and CD4 + CD25 + Th act activated helper T cells to values corresponding to the physiological norm. Conclusion BIV demonstrated notable hematopoietic- and T-lymphopoiesis-modulating activity. The compound partially restored erythropoiesis as well as central and peripheral T-lymphopoiesis, while providing balanced regulation of cytotoxic, regulatory, and memory T-cell subsets in cyclophosphamide-induced T-lymphopoiesis-suppressive models. Several evaluated T-lymphocyte subpopulations approached or returned to physiological control levels under the experimental conditions, although full translational validation requires further pharmacological and toxicological investigation.