||| Bangladesh Journal of Pharmacology |||

Prednisone inhibits osteosarcoma cell by regulating the Wnt/beta-catenin signaling pathway

2024-12-16T17:53:16+00:00

Prednisone, a synthetic glucocorticoid, possesses a moderate duration of action in the human body. To investigate the effect of prednisone on osteosarcoma cells in vitro, CCK8, wound healing, Transwell assays, flow-cytometry, western blot, and ELISA were used to measure cell proliferation, cell migration, cell invasion, cell cycle, cell apoptosis, and the key proteins in Wnt/beta-catenin pathway. The results showed prednisone could inhibit the proliferation in osteosarcoma cells and exhibit lower proliferation toxicity towards normal bone cells compared to cisplatin by 17.5% (p<0.001). Cell apoptosis was increased by 6.6 and 7.4%, cell migration was decreased to 62.6 and –23.9%, G0/G1 phase cells were increased by 33.0 and 17.9%, and S phase cells were reduced by 29.6 and 18.0% (all p<0.001) in Mg63 and Saos-2 cells respectively after prednisone treatment. The expressions of beta-catenin, cMYC, cyclin D1, and MMP7 were also reduced. In conclusion, prednisone inhibits osteosarcoma cells by regulating the Wnt/β-catenin signaling pathway.

Ginsenoside Rb1 ameliorates neutrophil extracellular traps-induced vascular endothelial damage by suppressing apoptosis

2024-12-16T18:08:52+00:00

The study aims to investigate the effect of ginsenoside Rb1 on improving neutrophil extracellular traps-induced vascular endothelial damage. The CCK8 assay was used to evaluate the impact of ginsenoside Rb1 on cell activity. Flow cytometry was used to assess cell apoptosis. E-cadherin was used to determine the damage to endothelial cells, and caspase 3 was used to detect apoptosis-related proteins. Ginsenoside Rb1 (100 umol/L) could significantly increase the cell viability (p<0.05). At this concentration, the damage caused by neutrophil extracellular traps to human umbilical vein endothelial cells could be reversed (p<0.05). Ginsenoside Rb1 (100 umol/L) could significantly inhibit the apoptosis and the expression of caspase3 protein caused by neutrophil extracellular traps (p<0.05). Ginsenoside Rb1 can reduce vascular endothelial injury induced by neutrophil extracellular traps, ginsenoside Rb1 protects vascular endothelium by inhibiting cell apoptosis.

Catalpol alleviates the lipopolysaccharide-induced inflammatory response of BV2 cells

2024-12-16T18:27:36+00:00

This study aimed to investigate the effect of catalpol on the inflammatory response of murine microglial cell line (BV2 cells) induced by lipopolysaccharide. Cell proliferation activity was detected by CCK-8 assay. The morphology of BV2 was observed by an optical microscope. The inflammatory factors interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were detected by enzyme‐linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) were detected by flow cytometry. Induced nitric oxide synthase (iNOS) level was detected by immunofluorescence. The results showed that 5 μg/mL catalpol did not effect the proliferation of BV2 cells, while 10 ug/mL catalpol significantly decreased the viability of BV2 cells. Then the experiment was carried out with 5 ug/mL catalpol. Catalpol can improve the morphology of lipopolysaccharide-induced BV2 cells, decrease the level of inflammatory factors, and reduce the production of iNOS and ROS. Therefore, catalpol can inhibit the lipopolysaccharide-induced activation of BV2 cells and has anti-inflammatory effects.

Total flavonoids of Abelmoschus manihot ameliorate lipid deposition in HK-2 cells by inhibiting fatty acid uptake mediated by CD36

2024-12-16T18:53:00+00:00

This study aimed to explore the mechanism by which total flavones of Abelmoschl manihot reduce intracellular lipid deposition in HK-2 cells (Human renal cortex proximal tubule epithelial cells) and thus reduce cell apoptosis. Palmitic acid was employed to induce intracellular lipid deposition. The cell proliferation activity was detected by the CCK-8 assay. The cell death status was evaluated by flow cytometry. The intracellular lipid deposition was observed by oil red O and BODIPY probe staining. The expression level of CD36 in HK-2 cells was determined by western blot. The results indicated that total flavones of A. manihot could inhibit the expression of CD36 in HK-2 cells in a dose-dependent manner and reduce lipid deposition. Consequently, total flavones of A. manihot protect HK-2 cells by reducing intracellular lipid deposition by inhibiting CD36-mediated fatty acid uptake.

Antibacterial effect of Dracaena indivisa leaf extracts

2024-12-16T17:24:04+00:00

No abstract