No abstract

Anti-cancer property of fungi derived β-glucan (Lentinula edodes) on several cancer cell lines have been reported. In this work, the SH-SY5Y cell lines were treated with various concentrations of β-glucan (62.5, 125, 250 and 500 μg/mL) and the viability of the cells was tested using the XTT assay after 24 hours. Cleaved PARP, BCL-2, 8-hydroxy-desoxyguanosine (8-oxo-dG), cleaved caspase 3, Bax, total oxidant, and total antioxidant levels in the cells were measured by commercial kits. β-Glucan significantly decreased the cell viability in SH-SY5Y cells. ELISA tests demonstrated that β-glucan therapy dramatically increased 8-oxo-dG, cleaved caspase 3, Bax, cleaved PARP, total oxidant. However, β-glucan treatment did not change the BCL-2 protein level. Altogether, β-glucan caused significant cytotoxicity in SH-SY5Y cells by inducing oxidative stress, increasing DNA damage, and ultimately increasing apoptosis.

Colorectal cancer is the third most lethal and fourth most commonly diagnosed cancer worldwide. Sinapic acid, a derivative of hydroxycinnamic acid, is a promising phytochemical exhibiting numerous pharmacological activities in various systems. It is a substantial chain-breaking antioxidant that operates as a radical scavenger. The aim of this research was to investigate the antiproliferative effect of sinapic acid on the HT-29 cell line, besides the mechanisms underlying this activity. The effect of sinapic acid on the viability of HT-29 cell line was investigated using XTT assay. the levels of BCL-2, cleaved caspase 3, BAX, cleaved PARP and 8-oxo-dG were measured using ELISA. Gamma-H2AX and cytochrome C expression was assessed semi-quantitatively using immunofluorescence staining. Sinapic acid at 200 μM and higher doses produced a significant antiproliferative effect on HT-29 cells. The IC50 value was found to be 317.5 μM for 24 hours. Sinapic acid (317.5 μM) significantly elevated cleaved caspase 3, BAX, cleaved PARP and 8-oxo-dG levels. the levels of γ-H2AX foci are significantly higher while the levels of cytochrome-C are lower in sinapic acid treated HT-29 cells. These results indicate that sinapic acid has an antiproliferative, apoptotic and genotoxic effect on colon cancer cells.

No abstract

The latest research has shown that the new generation of antiepileptic drugs has neuroprotective on nervous system. On the other hand, the effect of levetiracetam, a new generation antiepileptic drug, on GIC in SH-SY5Y cells remains uncertain. This research aims to investigate the effect of levetiracetam on GIC and oxidant and antioxidant levels in SH-SY5Y cells. It is utilized SH-SY5Y cell line at this research. Four groups were formed to assess the impact of levetiracetam on SH-SY5Y cell death following GIC. While no treatment was administered to the control group, 10 mM glutamate was administered to the glutamate group for 24 hours (10, 25, 50 and 100 μg/ml). LEV at different concentrations was given to the levetiracetam for 24 hours. The levetiracetam + glutamate was pretreated with levetiracetam at several concentrations for 1 hour (10, 25, 50, and 100 μg/ml), which was followed by a 24-hour exposure to 10 mM glutamate. TAS and TOS levels in cells and cell viability were examined. Following the GIC, a 25 μg/ml-Levetiracetam improved cell viability in neuroblastoma cells dramatically (p < 0.05). LEV (25 ug/ml) + glutamate while enhanced TAS levels in neuroblastoma cells in comparison to the glutamate (p < 0.05), significantly reduced TOS levels (p < 0.05 Levetiracetam improves cell survival by reducing cell death following GIC in neuroblastoma cells. In the acute process, levetiracetam exerts a protective effect.

BackgroundGambogic acid has demonstrated inhibitory effects on the growth of various cancer cell types, such as breast cancer, pancreatic cancer, prostate cancer, lung cancer, and osteosarcoma. This study aims to investigate the antiproliferative activity of Gambogic acid on SNU-16 cells derived from gastric signet ring cell carcinoma and elucidate the underlying mechanisms. Material and MethodsThe cytotoxic effect of gambogic acid was evaluated in SNU-16 cells by treating them with different concentrations of the compound, and the XTT cell viability assay was employed to assess cell viability.ELISA was used to measure bax, BCL-2, caspase 3, PARP, and 8-oxo-dG levels. Additionally, immuno uorescence staining was applied to assess 8-oxo-dG and LC3β levels in SNU-16 cells. ResultsIt was observed that gambogic acid exerted a dose-dependent and statistically signi cant antiproliferative effect on SNU-16 cells. The IC 50 value of gambogic acid in SNU-16 cells was found to be 655.1 nM for 24 hours. Subsequent investigations conducted using the IC 50 dose revealed a signi cant upregulation of apoptotic proteins including cleaved caspase 3, Bax, and cleaved PARP (p < 0.001), along with a downregulation of BCL-2 (p < 0.001), an anti-apoptotic protein. Moreover, the administration of this drug led to an upregulation of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicating oxidative damage in DNA, as well as an increase in LC3β levels (p < 0.05), a marker associated with autophagy. ConclusionThe antiproliferative effect of gambogic acid against gastric signet ring cell carcinoma is attributed to its ability to induce apoptosis and autophagy. This discovery highlights the promising potential of gambogic acid as a treatment option for gastric signet ring cell carcinoma.

Sugammadex (SUG) is a modified γ-cyclodextrin molecule used in patients under general anesthesia to reverse the effects of neuromuscular blocking agents. Besides, recent studies have shown that SUG has positive effects on the nervous system. However, its effect on seizures is still unclear. The current study aimed to examine the effects of SUG on pentylenetetrazole (PTZ)-induced epileptic seizures in mice. The mice were randomly divided into 4 groups. Group 1 was control, group 2 was administered saline (1 mL/kg serum physiologic), and Groups 3 and 4 were administered vortioxetine (150 and 300 mg/kg). Pentylenetetrazole (60 mg/kg) was given to induce seizures 30 min after saline or drug administration except for the control group. Total oxidant status (TOS) and total antioxidant status (TAS) levels in the hippocampus and cortex were measured using a commercial kit. 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), 3,3 dityrosine, caspase-3, apoptosis-inducing factor (AIF), and light chain 3 (LC3B) levels in the hippocampal CA1 region after seizures were evaluated immunohistochemical staining. SUG reduced seizure stages and increased epileptic seizure onset times. Moreover, it decreased TOS levels and increased TAS levels in the hippocampus and cortex. Besides, after seizures, it reduced 4-HNE, 3,3 dityrosandine, caspase-3, and LC3B immunohistochemical scores in the hippocampal CA1 region. SUG has protective effects on pentylenetetrazole-induced seizures in mice, with alleviated seizures, oxidative stress, apoptosis, and autophagy. The anticonvulsant mechanism of SUG may be related to the inhibition of the oxidative stress pathway.

Background Gambogic acid has demonstrated inhibitory effects on the growth of various cancer cell types, such as breast cancer, pancreatic cancer, prostate cancer, lung cancer, and osteosarcoma. This study aims to investigate the antiproliferative activity of Gambogic acid on SNU-16 cells derived from gastric signet ring cell carcinoma and elucidate the underlying mechanisms. Material and Methods The cytotoxic effect of gambogic acid was evaluated in SNU-16 cells by treating them with different concentrations of the compound, and the XTT cell viability assay was employed to assess cell viability. ELISA was used to measure bax, BCL-2, caspase 3, PARP, and 8-oxo-dG levels. Additionally, immunofluorescence staining was applied to assess 8-oxo-dG and LC3β levels in SNU-16 cells. Results It was observed that gambogic acid exerted a dose-dependent and statistically significant antiproliferative effect on SNU-16 cells. The IC50 value of gambogic acid in SNU-16 cells was found to be 655.1 nM for 24 hours. Subsequent investigations conducted using the IC50 dose revealed a significant upregulation of apoptotic proteins including cleaved caspase 3, Bax, and cleaved PARP (p < 0.001), along with a downregulation of BCL-2 (p < 0.001), an anti-apoptotic protein. Moreover, the administration of this drug led to an upregulation of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicating oxidative damage in DNA, as well as an increase in LC3β levels (p < 0.05), a marker associated with autophagy. Conclusion The antiproliferative effect of gambogic acid against gastric signet ring cell carcinoma is attributed to its ability to induce apoptosis and autophagy. This discovery highlights the promising potential of gambogic acid as a treatment option for gastric signet ring cell carcinoma.