Scopoletin protects INS-1 pancreatic β cells from glucotoxicity by reducing oxidative stress and apoptosis

This study investigated whether scopoletin could protect INS-1 pancreatic beta cells from apoptosis and oxidative stress caused by high glucose. Cells were pretreated with glucose (5.5 or 30 mM) and then treated with 0, 5, 10, 25, or 50 mu M Scopoletin. Cell viability and insulin secretion were measured in addition to ROS, TBARS, NO and antioxidant enzymes. Western blot analysis and flow cytometric assessment of apoptosis were also carried out. High glucose of 30 mM caused glucotoxicity and cell death in INS-1 pancreatic beta cells. However, 5, 10, 25 or 50 mu M scopoletin increased the level of cell viability as concentrations increased. The levels of ROS, TBARS, and NO increased by high glucose were significantly decreased after scopoletin treatment. Scopoletin also raised antioxidant enzyme activities up against oxidative stress produced by high glucose. These effects influenced the apoptosis pathway, raising levels of anti-apoptotic protein, Bcl-2, and reducing levels of pro-apoptotic proteins, including JNK, Bax, cytochrome C, and caspase 9. Annexin V/propidium staining indicated that scopoletin significantly lowered high glucose-produced apoptosis. These results indicate that scopoletin can protect INS-1 pancreatic beta cells from glucotoxicity caused by high glucose and have potential as a pharmaceutical material to protect the pancreatic beta cells.

Automated summary

This study found that scopoletin can protect INS-1 pancreatic beta cells from apoptosis and oxidative stress caused by high glucose. It does so by reducing ROS, TBARS, and NO levels, increasing antioxidant enzyme activities, and influencing the apoptosis pathway. These findings suggest that scopoletin has the potential to be used as a pharmaceutical material to protect pancreatic beta cells.