The purpose of this study was to investigate the phytochemical analysis of D. pentaphyllum and its cytotoxic activity on human cervical cancer (HeLa) cells with possible mechanisms. Total phenolic contents (TPC) and phytochemical analysis of the extract were evaluated using spectrophotometric method and RP-HPLC, respectively. The cytotoxic effect of the extract was evaluated using the MTT assay. The mechanism of the cytotoxic effect of the extract was also evaluated in terms of apoptosis, cell cycle, and mitochondrial membrane potential (MMP) using the fluorometric methods. The TPC of the extract was calculated as 68.9±2.3 mg gallic acid equivalent per g sample and quercetin was determined as the major phenolic in the extract. The extract showed a selective cytotoxic effect (6.5-fold) on HeLa cells compared to normal fibroblast cells. The cytotoxic effect of the extract was found to be due to the arresting of the cell cycle in the S phase and increasing apoptosis through decreased MMP. Further studies are needed for the comprehensive effects of the extract on cell signaling.

Acute myeloid leukemia (LAML) is one of the most prevalent hematological malignancies. In recent years, while targeted approaches have shown promise in the fight against cancer, the treatability and prognosis of patients remain inadequate due to the shortage of drugs. Noncoding RNAs, especially circular RNA (circRNA) and microRNA (miRNA), have been shown to play a unique role in tumor development. This study aims to identify the disease-associated circRNA–miRNA–mRNA network by bioinformatic analysis and investigate the mechanisms in the development and progression of LAML. Additionally, it reveals the promising roles of these molecules as a diagnostic biomarker and therapeutic target for LAML treatment. Using various bioinformatics approaches, we identified the hsa_circ_0058058/miR-324-5p axis in LAML and its possible functions in LAML development. According to our results, hsa circ-0058058 can regulate the expression of AP1G1 and SP1 through miR-324-5p to support angiogenesis, the cell cycle, and DNA replication processes. Downregulation of hsa circ-0058058 may contribute to the anticancer functions of miR-324-5p on LAML tumorigenesis, and upregulation of miR-324-5p can abolish the oncogenic effects of AP1G1 and SP1 on LAML tumorigenesis. Additionally, highly enriched pathways indicated possible interactions between molecules underlying LAML pathology. Targeted molecules within this network may be able to function as therapeutic and diagnostic biomarkers for disease, while more research and clinical confirmation are needed.

Background: Postprandial lipemia (PPL) causes endothelial dysfunction by causing endothelial damage to lipoproteins that remain rich in triglycerides. Endocan is a proteoglycan with increased tissue expression, endothelial activation, and neovascularization. The aim of the study was to examine circulating endocan levels in PPL subjects by considering the degree of PPL response according to a high-fat test meal. The other aim was to determine the association between endocan levels and endothelial and inflammatory factors. Method: Fifty-four hyperlipidemic subjects and 28 normolipidemic subjects consumed the high-fat meal. Endocan, sICAM-1, sVCAM-1, and VEGFA as endothelial factors and IL-6 and LFA-1α as inflammatory factors were evaluated. Results: Fasting serum endocan, VEGFA, sICAM-1, sVCAM-1 IL-6, and LFA-1α levels were increased in the PPL group compared to the control group. The PPL group was divided into tertiles based on mean AUC levels. Endocan levels in tertile 3 were at the highest and were increased significantly compared to tertiles 1 and 2. AUC and endocan levels were positively correlated with other endothelial and inflammation factors. ROC analysis showed endocan levels to be one of the highest values. Conclusions: Circulating endocan is seen at significantly higher levels and independently associated with endothelial and inflammatory factors in postprandial lipemia and dyslipidemia.

Antineoplastic agents can induce tissue damage through oxidative stress mechanisms. Doxorubicin, a widely used chemotherapeutic agent, has been shown to cause permanent damage to reproductive tissues. Antioxidant‐rich dietary interventions are considered a promising approach to mitigate oxidative stress‐related damage. This study aimed to evaluate the therapeutic potential of an antioxidant‐rich bee product mixture (ARPM) in ameliorating doxorubicin‐induced ovarian injury. The ARPM, composed of honey, pollen, propolis, and royal jelly, was administered via gavage to female Sprague‐Dawley rats (180–200 g) following chronic ovarian damage induced by doxorubicin (6 mg/kg, ip). Oxidative stress markers, including superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH), as well as endoplasmic reticulum (ER) stress‐related markers such as 78‐kDa glucose‐regulated protein (GRP78), inositol‐requiring enzyme 1 (IRE1), C/EBP homologous protein (CHOP), tumor necrosis factor‐alpha (TNF‐α), and caspase‐3, were simultaneously evaluated. In addition, estradiol (E2) and progesterone levels were measured, and histopathological evaluations were conducted. The mixture, rich in bioactive compounds including chrysin, pinocembrin, caffeic acid, ferulic acid, and coumaric acid, was found to significantly improve ovarian function by reducing ER stress compared to the control group. These findings suggest that ARPM may offer protective effects against doxorubicin‐induced ovarian damage through its antioxidative and anti‐ER stress properties.