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.

Association of Different Doses of Curcumin with Preadipocyte to Adipocyte Differentiation - Medical Journal of Bakirkoy

Human adipose tissue is involved in fat storage and also plays a role in the immune response. Curcumin (CUR), a natural polyphenol is suggested to supress adipocyte differentiation in the early stage by inhibiting secretion of some regulators and the inflammatory cytokines and by activating the secretion of antiinflammatory cytokines. Our aim in this research was to examine the molecular pathways of the inhibitory effects of different doses of curcumin (0.5 µM, 5 µM, 10 µM, 20 µM, 50 µM) on the preadipocyte-adipocyte differentiation and the anti-inflammatory effect of curcumin for preventing adipocyte related oxidative and inflammatory status. Differentiation of cells was performed using Oil red O, mRNA expression levels of adiponectin, CCAAT/enhancer binding proteinα (C/EBPα), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), leptin, Nuclear Factor kappa B1 (NFκB1), peroxisome proliferator-activated receptor gamma (PPARγ), sirtuin-1 (SIRT-1), tumor necrosis factor-α (TNF-α), transient receptor potential vanilloid receptor1 (TRPV1), uncoupling protein2 (UCP2), vasculer endothelial growth factor-A (VEGF-A), vascular endothelial growth factor receptor I (VEGF-RI), VEGF-RII were evaluated in preadipocytes and adipocytes. Curcumin suppressed the differentiation of preadipocyte to adipocytes, decreased the release of proinflammatory cytokines, but it did this by regulating C/EBPα and PPARγ gene expressions outside the NF-κB pathway. Curcumin effectively suppressed adipogenic transcription factors and also adipocyte differentiation at all doses between 0.5–50 µM, but showed its anti-inflammatory effect especially in the application of curcumin of 50 µM.

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.

Objective: In recent years due to their natural ingredients phytotherapeutic sources have become increasingly needed as alternatives to chemotherapeutic drugs. Avocado and peanut were shown to contain diverse bioactive compounds exhibit anti-oxidant, anti-inflammatory and anti-proliferative effects. We aimed to determine and compare the anticarcinogenic effects of Bacon and Fuerte avocado, Osmaniye peanuts on the inhibition the viability of human prostate carcinoma (PC3) and human lung carcinoma (A549) cells. Methods: Three kilograms of avocados and peanuts were purchased domestically produced. Avocados and peanuts were divided into three parts. Avocado and peanut parts were dissolved in 96% and 60% ethanol. A549 and PC3 cells were incubated with 200μg/ml ethanol extracts of avocados and peanuts for 24 hours. PC3 and A549 cancer cell viability analysis was performed using CCK-8 Kit. Results: All parts of Bacon and Fuerte avocado were cultured with A549 and PC3 cells caused decrease in the viability of both cancer cells. All parts of peanut caused decrease in viability of A549 but there was no difference for PC3. Also, the peel and seed parts in 96% ethanol of Bacon and Fuerte avocado caused more decrease than pulp part for A549 and PC3. The inner peel and kernel parts in 96% ethanol of peanut caused more decrease than outer peel part for A549 but there was no difference for PC3. Conclusion: Peel and seed parts of avocados and outer sheel and kernel parts of peanuts can serve as valuable sources to reduce cancer cell viability.