International Journal of Pharmaceutics, Journal Year: 2024, Volume and Issue: unknown, P. 125005 - 125005
Published: Nov. 1, 2024
Language: Английский
International Journal of Pharmaceutics, Journal Year: 2024, Volume and Issue: unknown, P. 125005 - 125005
Published: Nov. 1, 2024
Language: Английский
Journal of Controlled Release, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0Frontiers in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 12
Published: Feb. 26, 2025
The molecular mechanisms underlying cardioprotection against doxorubicin (DOX)-induced myocardial injury are poorly understood. Histone deacetylase 2 (HDAC2) plays a significant role in oxidative stress, apoptosis, and mitochondrial dysfunction is implicated many human diseases, This study investigated the relationship between HDAC2 expression DOX-induced using vivo rat model of cardiotoxicity vitro experiments with H9c2 cardiomyocytes. was established by administering DOX via intraperitoneal injections. suppressed rats sodium butyrate (SB) Echocardiography measurements were performed at baseline on day 15 post-treatment. euthanized cardiac tissues harvested. tissue samples analyzed hematoxylin eosin H&E staining, immunohistochemistry, Masson Sirius Red TUNEL western blotting to determine status apoptosis. In experiments, cells treated DOX. or transfected shRNA knockdown (shHDAC2). from different groups Rt-qPCR, CCK-8 cell viability assay, cardiomyocyte treatment induced rats. DOX-treated showed significantly higher levels compared corresponding controls. However, inhibition mitigated suggested strong association injury. cells, shHDAC2 alleviated apoptosis enhacing AKT phosphorylation. These findings demonstrated that silencing protected activating PI3K/AKT signaling pathway. Suppressing Therefore, promising therapeutic target for mitigating
Language: Английский
Citations
0Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
5-Aminolevulinic acid (5-ALA)-based photodynamic therapy (PDT) has demonstrated considerable potential in breast cancer treatment. However, its efficacy is limited by low tissue selectivity and the rapid conversion of 5-ALA to non-photosensitive heme tumor tissues, reducing therapeutic effectiveness. This study aims develop a multifunctional nanomedicine enhance 5-ALA's PDT while introducing chemodynamic (CDT) for synergistic inhibition. By designing zinc-ion-doped cuprous metal-organic framework (MOF) nanocarrier loaded with (5-ALA@Zn-CuTz), we seek improve targeting, prolong photosensitizer retention, outcomes. To biocompatibility active surface 5-ALA@Zn-CuTz nanoparticles (NPs) was modified platelet membrane (PM), forming 5-ALA@Zn-CuTz@PM NPs. The evaluated vitro vivo using mice models. Cellular uptake, reactive oxygen species (ROS) generation, inhibition efficiency were analyzed through fluorescence imaging, biochemical assays, histological analysis. Upon intravenous administration, NPs selectively accumulated cells. Within tumor, Zn2+ bound intracellular protoporphyrin IX (PpIX) form PpIX-Zn, inhibiting oxygenase-1 (HO-1) activity preventing PpIX into heme. increased effective concentration photosensitizer, thereby enhancing PDT. Additionally, Cu+ catalyzed decomposition excess H2O2 microenvironment, generating hydroxyl radicals, which alleviated hypoxia activated CDT. PDT/CDT effect significantly enhanced growth vivo. effectively selective targeting HO-1 simultaneously leveraging CDT additional suppression. combined strategy superior outcomes, highlighting this nanoplatform as promising approach
Language: Английский
Citations
0International Journal of Pharmaceutics, Journal Year: 2024, Volume and Issue: unknown, P. 125005 - 125005
Published: Nov. 1, 2024
Language: Английский
Citations
0