Introduction: Insulin resistance is associated with a pro-inflammatory state increasing the risk for complications in patients with type 2 diabetes mellitus (T2DM). In addition to its chronobiotic effects, the pineal hormone melatonin is known to exert anti-inflammatory and antioxidant effects. Melatonin was also suggested to affect insulin secretion. The aim of this study was therefore to investigate the effect of melatonin on inflammation in diabetic rats and to study the possible involvement of the melatonin receptor, MT2. Materials and Methods: Male Sprague Dawley rats were randomly divided into four experimental groups (n = 10 per group): (1) control, (2) streptozotocin/nicotinamide induced diabetes type 2 (T2DM), (3) T2DM treated with melatonin (500 µg/kg/day), and (4) T2DM treated with melatonin (500 µg/kg/day for 6 weeks) and the selective MT2 receptor antagonist luzindole (0.25 g/kg/day for 6 weeks). Blood samples were taken for biochemical parameters and various tissue samples (liver, adipose tissue, brain) were removed for immunohistochemistry (IHC), Western blot (WB), and Q-PCR analyses, respectively. Results: Melatonin significantly reduced increased blood levels of liver transaminases (AST, ALT), blood urea nitrogen (BUN), triglyceride, very low-density lipoprotein (VLDL), and cholesterol in diabetic rats with luzindole treatment partly reversing this effect regarding the lipids. Furthermore, the liver and adipose tissues of T2DM rats treated with melatonin showed lower expression of the inflammatory markers IL-1β, IL-6, TNF-α, and NF-κB as compared to the T2DM group without melatonin. The results also showed that the MT2 receptor is at least partly involved in the protective effects of melatonin. Conclusions: Our results suggest that melatonin exerts relevant anti-inflammatory effects on various tissues in type 2 diabetic rats.

Background: Glioblastoma multiforme (GBM) is the most aggressive and fatal primary brain tumor, characterized by rapid proliferation, resistance to therapy, and poor prognosis. Current treatment strategies, including surgery, radiotherapy, and chemotherapy, have limited efficacy and significant side effects. Phytotherapeutic agents such as thymoquinone (TQ), the major bioactive compound of Nigella sativa, have gained attention for their potential anticancer properties. TQ has been reported to exhibit pro-apoptotic, anti-inflammatory, and anti-proliferative effects in various cancer models. Objective: This study aimed to investigate the apoptotic effects of TQ on U87 human glioblastoma cells by evaluating its impact on cell viability, migration, colony formation, and the expression of key genes and proteins involved in apoptosis and inflammation. Methods: U87 glioblastoma cells were treated with increasing concentrations of TQ (10–100 µM) for 24, 48, and 72 h. Cell viability was assessed using the Sulforhodamine B (SRB) assay. A scratch assay was performed to evaluate cell migration, and a colony formation assay was used to assess clonogenic potential. Quantitative real-time PCR (qRT-PCR) and Western blotting were conducted to analyze the expression levels of genes and proteins associated with apoptosis, inflammation, and cell cycle regulation. Results: TQ treatment significantly reduced U87 cell viability in a time- and dose-dependent manner, with IC50 values of 75 µM at 24 h, 45 µM at 48 h, and 36 µM at 72 h. The scratch assay demonstrated that TQ had no significant effect on U87 cell migration. Colony formation was inhibited at 10 µM after 24 h. qRT-PCR analysis revealed that at 50 µM TQ, caspase-3 and Bax mRNA levels were significantly upregulated. At 75 µM, caspase-9, caspase-3, Bax, and p21 mRNA levels increased, while caspase-8, Bcl-2, and Akt1 expression decreased. Western blot analysis showed increased expression of cleaved caspase-3, p21, and ATG5 proteins, along with decreased expression of caspase-8 and TNF-α at 24 h. Conclusion: TQ exhibits potent pro-apoptotic effects in U87 glioblastoma cells by modulating key apoptotic and inflammatory pathways, including the PI3K/AKT signaling axis. These findings suggest that TQ may serve as a promising adjuvant therapeutic agent for GBM. Further studies are required to elucidate its full molecular mechanisms and potential clinical applications.

The present study aims to investigate the changes in the expression levels of miR-675 and some selenoproteins (Sel K, Sel W, and Sel P) in patients with breast cancer, before and after radiotherapy. This study included 35 breast cancer patients who applied to the Department of Radiation Oncology for radiotherapy and 25 healthy female controls. miR-675 expressions were analyzed by using quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Western blot was conducted to determine Sel K, Sel W, and Sel P expression levels. Biochemical parameters and complete blood count were analyzed by autoanalyzer system and automatic cell counter, respectively. Plasma Sel K protein expression levels were decreased in the after-radiotherapy group compared to the control and before-radiotherapy groups, but plasma miR-675 expression levels were lower in both before and after radiotherapy groups compared to the control group. Our findings showed that miR-675 and Sel K expression levels changed after radiotherapy in breast cancer patients. These changes may have the potential to be biomarkers for the effectiveness of radiotherapy in breast cancer.

Background/Objectives: Oxidative stress is a key contributor to breast cancer (BC) progression and therapeutic response. Although carboplatin is widely used in BC treatment, the effects of combining carboplatin with metformin and boric acid (BA) on cellular redox homeostasis remain poorly understood. This study investigated the effects of these agents on cell viability, migration, and oxidative stress in BC and normal mammary epithelial cells. Methods: Human BC MCF-7 cells and normal mammary epithelial CRL-4010 cells were treated with carboplatin, metformin, BA, and selected combination regimens. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay following 24, 48, and 72 h of treatment. Cell migration was evaluated using a scratch wound-healing assay, and intracellular oxidative stress responses were assessed by measuring superoxide dismutase (SOD) activity. Statistical analyses were performed using one-way ANOVA followed by Fisher’s least significant difference (LSD) post hoc test. Results: Treatment responses were both time- and treatment-dependent in MCF-7 and CRL-4010 cells. Combination regimens significantly reduced cell viability after 48 and 72 h (all p < 0.0001) and generally exhibited greater inhibitory effects than single-agent treatments. Metformin- and BA-containing combinations also produced more pronounced inhibition of cell migration. Significant treatment-related alterations in SOD activity were observed in both cell lines, indicating treatment-associated changes in antioxidant enzyme activity. While several combination regimens decreased SOD activity, others induced increased SOD activity, suggesting differential oxidative stress responses between malignant and non-malignant cells. Conclusions: Carboplatin, metformin, and BA significantly modulated cell viability, migration, and antioxidant responses in both BC and normal mammary epithelial cells. Combination treatments generally produced greater inhibitory effects on cell viability and migration than selected single-agent treatments, particularly in MCF-7 cells. These findings demonstrate treatment-dependent changes in cell viability, migration, and SOD activity and provide a basis for further investigation of the molecular mechanisms underlying carboplatin-based combination treatments.

Chronic alcohol consumption exacerbates kidney injury, particularly in individuals with hepatitis B virus (HBV) infection. This study investigated the protective effects of boric acid supplementation against alcohol-induced renal damage in HBV transgenic mice. HBV transgenic mice were divided into four groups: control (C), boric acid (B), alcohol (A), and alcohol + boric acid (A + B). Renal injury was evaluated using H&E, PAS, TUNEL, and desmin staining. The expression of caspase-3, cytochrome c, and APAF-1 was analyzed by qRT-PCR. Biochemical analyses included BUN, creatinine, oxidative stress markers (ROS, MDA, TOS, OSI), total antioxidant status, and antioxidant enzyme activities (SOD, CAT, GPx). Histopathological findings showed activated parietal epithelial cells in all groups, indicating renal injury. Alcohol significantly increased tubular damage, podocyte desmin expression, apoptosis, cytochrome c and APAF-1 mRNA levels, and oxidative stress markers, while reducing antioxidant enzyme activities and BUN levels compared with controls. Boric acid supplementation significantly mitigated alcohol-induced tubular injury, apoptosis, oxidative stress, and serum creatinine levels, and improved BUN values. Boric acid treatment alone also alleviated glomerular and tubular injury and reduced tubular apoptosis compared with HBV control mice. Overall, boric acid exerts renoprotective effects in HBV-transgenic mice subjected to chronic alcohol exposure by inhibiting oxidative stress, apoptosis, and podocyte injury.