Nanoparticles are attracting attention for their potential therapeutic applications, particularly in cancer therapy, underscoring their importance in medicine. Cadmium sulfide nanoparticles, known for their robust catalytic and optical properties, are classified as chalcogenides and show promise for cancer diagnosis and treatment. Neuroblastoma, a common solid tumor in childhood, poses a significant health threat with different outcomes depending on its biological subtype. This study evaluated the antiproliferative effects of cadmium sulfide nanoparticles on the SY-SH5Y cell line. Walnut shell extract and Na₂S were used to facilitate the synthesis of cadmium sulfide nanoparticles by green synthesis. Characterization of the synthesized cadmium sulfide nanoparticles was performed by Fourier transform infrared spectroscopy, scanning electron microscopy, and x-ray diffraction analyses. The SH-SY5Y cell line was cultured in a standard cell culture medium and then exposed to different cadmium sulfide nanoparticles (10–25–50–75–100 µg/mL) for 24 hours. Cell viability, oxidant, and antioxidant levels were then assessed using a 3-(4,5-dimetiltiyazol-2-il)-2,5-difeniltetrazolyum bromür, total antioxidant, and total oxidant assays. The data showed that applying 100 μg/mL cadmium sulfide nanoparticles resulted in a significant decrease in cancer cell viability of up to 40.96 % (p<0.05). The cadmium sulfide nanoparticles had a dose-dependent effect on the SH-SY5Y cell line. Furthermore, cadmium sulfide nanoparticles increased oxidative activity in neuroblastoma cells, which was consistent with the results of the 3-(4,5-dimetiltiyazol-2-il)-2,5-difeniltetrazolyum bromür assay. In conclusion, cadmium sulfide nanoparticles exhibited potent activity against the neuroblastoma cell. This study highlights the antiproliferative efficacy of green-synthesized cadmium sulfide nanoparticles with walnut shell extract on relevant cancer cell lines.

Objective: This study aimed to evaluate the antiproliferative effects of lacidipine, a dihydropyridine-derived L-type calcium channel blocker, on the human colon cancer cell line (SW480) and the associated changes in inflammatory and oxidative stress markers. Materials and Methods: SW480 cells were exposed to lacidipine doses ranging from 100 to 250 µg/mL. Cytotoxicity was assessed using the MTT assay. Oxidative stress levels were measured using TAC and TOS parameters, while the inflammatory response was assessed using ELISA for IL-1β, TNF-α, and TGF-β levels. Results: Lacidipine exhibited significant cytotoxic effects at a dose of 100 µg/mL, but increased cell viability was observed at higher doses. No statistically significant changes were observed in TAC and TOS levels. However, a significant decrease in IL-1β, TNF-α, and TGF-β levels was detected due to lacidipine; the most effective dose was determined to be 150 µg/mL. Conclusion: Lacidipine may have an antiproliferative effect by reducing inflammatory cytokine levels in SW480 colon cancer cells. These findings support the potential anticancer effect of lacidipine related to its anti-inflammatory properties, and further preclinical studies are needed to elucidate its mechanisms.

OBJECTİVE: In this study, it was aimed to evaluate the antineoplastic efficacy of Teranecron, which is frequently used in veterinary medicine, on human colorectal adenocarcinoma. MATERİALS AND METHODS: Teranecron (TRN) was used to evaluate its effectiveness in the study, and the antineoplastic drug Doxorubicin was used as a positive control. The cytotoxic activity of Teranecron on the human colorectal cell line CaCo-2 was investigated. MTT proliferation test was used to determine the viability rates. ANOVA Tukey test was used for statistical analysis and the level of significance was accepted as P<0.01. RESULTS: When we performed viability tests, it was observed that the toxicity of Teranecron increased in a dose-dependent manner in the groups in which Teranecron was administered alone. While the viability of CaCo-2 at 10 µM concentration was 94%, the viability rate at 100 µM concentration decreased to 79%. The viability was determined as 78.72% in the Dox 40 µM concentration, which we applied only as a positive control, and 73% in the group in which Dox 40 µM + TRN 100 µM was applied. In the groups where Dox+TRN was administered together, the toxic effect ratio started to increase depending on the concentration, starting from the TRN 50 µM dose. RESULTS: As a result of the viability test of teranecron on the CaCo-2 cell line, it was determined that the cytotoxic activity of TRN increased in a dose-dependent manner. When teranechron efficacy was compared with Doxorubicin used as an antineoplastic drug, it was determined that 75 µM TRN had the same effect as 40 µM Dox. Considering the side-effect profiles, TRN with fewer side effects seems to have the potential to be an alternative treatment for human colorectal cancer. More detailed studies are needed to recommend the use of TRN as an anticancer therapy. AMAÇ: Bu çalışmada veteriner hekimlikte sıklıkla kullanılan Teranekronun insan kolorektal adenokarsinomu üzerinde antineoplastik etkinliğinin değerlendirilmesi amaçlandı. GEREÇ VE YÖNTEM: Çalışmada etkinliğini değerlendirmek için Teranekron (TRN) ve pozitif kontrol olarak da antineoplastik ilaç olan Doksorubisin kullanıldı. İnsan kolorektal hücre hattı CaCo-2 üzerinde Teranekronun sitotoksik etkinliği araştırıldı. Canlılık oranları belirlenmesinde MTT proliferasyonu testi uygulandı. İstatistiksel analizler için ise ANOVA Tukey testi kullanıldı ve anlamlılık düzeyi P<0,01 olarak kabul edildi. BULGULAR: Canlılık testleri yaptığımızda Teranekronun tek olarak uygulandığı gruplarda Teranekronun doza bağlı olarak toksisitesinin arttığı görüldü. 10 µM konsantrasyonda CaCo-2 canlılığı %94 iken 100 µM’lık konsantrasyonda canlılık oranı % 79 a düştü. Sadece pozitif kontrol olarak uyguladığımız Dox 40 µM konsantrasyonunda canlılık %78,72 Dox 40 µM + TRN 100 µM uygulandığı grupta ise canlılık oranı %73 olarak belirlendi. Dox+TRN’nin birlikte uygulandığı gruplarda TRN 50 µM dozundan itibaren toksik etki oranı konsantrasyona bağlı olarak artmaya başladı. SONUÇLAR: Teranekronun CaCo-2 hücre hattı üzerinde yapılan canlılık testi sonucunda doza bağlı olarak TRN’nin sitotoksik etkinliğinin arttığı belirlendi. Teranekron etkinliği antineoplastik ilaç olarak kullanılan Doksorubisin ile karşılaştırıldığında ise 75 µM TRN’nin 40 µM Dox ile aynı etki ortay çıkarttığı belirlendi. Yan etki profilleri düşünülecek olursa daha az yan etki gösteren TRN insan kolorektal kanser tedavisinde alternatif bir tedavi olma potansiyeli olduğu görülmektedir. TRN’nin antikanser tedavisi kullanılmasının tavsiye edilmesi için daha detaylı çalışmalara ihtiyaç bulunmaktadır.

Girardinia diversifolia L. (Giant nettle) has similar characteristics to nettle (Urtica diocia L.) in the Urticaceae family. G. diversifolia L. is a plant used in traditional medicine for many medical conditions ranging from animal bites to infections. However, studies on the medical uses of giant nettle in the literature are extremely limited. In this study, giant nettle seedlings were grown, and root, leaf, and flower samples were taken at appropriate times. Water and methanol extracts were then obtained. Subsequently, plant extracts were tested in an in vitro wound healing model to investigate the effects of G. diversifolia L. on wound healing. The MTT cytotoxicity test was used to determine the effects of the relevant extracts on cell viability. In addition, ELISA tests were performed to determine the oxidative/antioxidative properties, as well as the biochemical properties, of wound tissue development (IL-1β, TNF-α, and TGF-β). The results were analyzed using the IBM SPSS 21.0 program. As a result of the analyses, it was observed that the flower extract of G. diversifolia L. obtained in methanol increased cell proliferation but had no effect on cell migration. It was determined that IL-1β levels increased with the increase in extract dose. In the cell culture wound model test, it was determined that TNF-α and TGF-β levels increased in the methanol flower extract groups at 250 µg/mL and 500 µg/mL, where migration was detected, while no change was observed in the other groups. It was also determined that antioxidant status increased depending on the dose.

Background: Alterations in glutamatergic homeostasis have been implicated in Alzheimer’s disease, but the relationship between total hippocampal tissue glutamate and Alzheimer-like molecular alterations remains unclear. This study evaluated the early neuroprotective potential of gentisic acid (GA) and erucic acid (EA) in an intracerebroventricular streptozotocin (icv-STZ)-induced rat model of sporadic Alzheimer-like pathology. Methods: Sixty-four female Sprague–Dawley rats were randomly assigned to eight groups: control, sham, STZ, STZ + GA (100 or 200 mg/kg/day), STZ + EA (25 or 50 mg/kg/day), and STZ + memantine (10 mg/kg/day). Treatments began immediately after STZ and continued orally for 21 days. Behavioral performance was assessed by Morris water maze and passive avoidance tests. Total hippocampal tissue glutamate was quantified by LC–MS/MS. Neuronal degeneration was assessed histopathologically, whereas tau, amyloid-β, and AChE immunoreactivity and tau-, APP-, and AChE-related in situ hybridization signals were evaluated. Results: Compared with controls, STZ-treated rats exhibited poorer behavioral performance, higher total hippocampal tissue glutamate, greater neuronal degeneration, and increased molecular signals. GA and EA administration was associated with attenuation of these alterations, with generally stronger effects at higher doses. EA at 50 mg/kg/day showed the lowest mean total hippocampal tissue glutamate among treatment groups. GA at 200 mg/kg/day and EA at 50 mg/kg/day showed the most consistent preservation across behavioral, histopathological, and molecular endpoints. Conclusions: Early GA and EA administration was associated with neuroprotective effects in the icv-STZ model. Because treatment began immediately after STZ administration, the findings support early or preventive neuroprotection rather than reversal of established Alzheimer-like pathology. Total tissue glutamate measurements neither distinguish extracellular glutamate nor directly demonstrate glutamate-mediated excitotoxicity.