Hyperinsulinemia occurs in type 2 diabetic patients with insulin resistance. This increase in insulin levels in the blood increases reactive oxygen species production and oxidative stress, resulting in DNA damage. Carvedilol (CRV) is a non-selective beta-blocker, and research has shown that this compound and its metabolites have anti-oxidative properties. Carvedilol can, directly and indirectly, reduce reactive oxygen species (ROS) and has a protective effect on DNA damage from oxidative stress. Given the insolubility of CRV in water, finding new methods to increase its solubility can be an essential step in research. This study aimed to determine whether carvedilol could have a protective effect on insulin-induced genomic damage. We treated cells with insulin alone, amorphous-CRV alone, and amorphous-CRV and niosomal-CRV with insulin and DNA damage were investigated using the comet method to achieve this goal. Our results showed that insulin in the studied concentration has a significant genotoxic effect and non-cytotoxic at higher concentrations. CRV, both in amorphous and niosome form, reduced insulin-induced DNA damage by reducing ROS production. The comet assay results demonstrate that treating HUVEC cells in pretreatment condition with amorphous-CRV and niosome-CRV significantly reduces DNA damage of insulin.
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http://dx.doi.org/10.1177/09603271211036124 | DOI Listing |
Biomaterials
January 2025
Department of Pharmacy of Puning People's Hospital (Guangdong Postdoctoral Innovation Practice Base of Jinan University), Department of Chemistry, State Key Laboratory of Bioactive Molecules and Druggability Assessment, MOE Key Laboratory of Tumor Molecular Biology, Jinan University, Guangdong, 510632, China. Electronic address:
Developing translational nanoradiosensitizers with multiple activities in sensitizing tumor cells and re-shaping tumor immunosuppressive microenvironments are urgently desired for addressing the poor therapeutic efficacy of radiotherapy in clinic. Inspired by the anaerobic and immunoagonist properties of the probiotic (bifidobacterium longum, BL), herein, a biomimetic Selenium nanoradiosensitizer in situ-formed on the surface of the probiotic (BL@SeNPs) is developed in a facile method to potentiate radiotherapy. BL@SeNPs selectively target to hypoxia regions of tumors and then anchor on the surface of tumor cells to inhibit its proliferation.
View Article and Find Full Text PDFMol Plant
January 2025
State Key Laboratory of Wheat Improvement, School of Advanced Agricultural Sciences, Peking University, Beijing 100871, China; Beijing Life Science Academy, Beijing 102299, China. Electronic address:
It has been hypothesized that DNA damage has the potential to induce DNA hypermethylation, contributing to carcinogenesis in mammals. However, there is no sufficient evidence to support that DNA damage can cause genome-wide DNA hypermethylation. Here, we demonstrated that DNA single-strand breaks with 3'-blocked ends (DNA 3'-blocks) can not only reinforce DNA methylation at normally methylated loci but also can induce DNA methylation at normally nonmethylated loci in plants.
View Article and Find Full Text PDFReprod Biol Endocrinol
January 2025
Reproductive Medicine Center, Zhuhai Maternal and Child Health Care Hospital, 543 Ningxi Road, Zhuhai, 519000, China.
Purpose: Prior sperm DNA fragmentation index (DFI) thresholds for diagnosing male infertility and predicting assisted reproduction technology (ART) outcomes fluctuated between 15 and 30%, with no agreed standard. This study aimed to evaluate the impact of the sperm DFI on early embryonic development during ART treatments and establish appropriate DFI cut-off values.
Methods: Retrospectively analyzed 913 couple's ART cycles from 2021 to 2022, encompassing 1,476 IVF and 295 ICSI cycles, following strict criteria.
Cell Commun Signal
January 2025
Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Background: Ovarian cancer (OC), particularly high-grade serous ovarian carcinoma (HGSOC), is the leading cause of mortality from gynecological malignancies worldwide. Despite the initial effectiveness of treatment, acquired resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) represents a major challenge for the clinical management of HGSOC, highlighting the necessity for the development of novel therapeutic strategies. This study investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a pivotal regulator of glycolysis, in PARPi resistance and explored its potential as a therapeutic target to overcome PARPi resistance.
View Article and Find Full Text PDFSci Rep
January 2025
Center of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
An ideal chemotherapeutic agent damages DNA, specifically in cancer cells, without harming normal cells. Recently, we used Box A of HMGB1 plasmid as molecular scissors to produce DNA gaps in normal cells. The DNA gap relieves DNA tension and increases DNA strength, preventing DNA double-strand breaks (DSBs).
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