Effects of Nigella sativa and thymoquinone on biochemical and subcellular changes in pancreatic β-cells of streptozotocin-induced diabetic rats.

BACKGROUND: The present study investigated the effects of Nigella sativa aqueous extract and oil, as well as thymoquinone, on serum insulin and glucose concentrations in streptozotocin (STZ) diabetic rats.

METHODS: Rats were divided into five experimental groups (control, untreated STZ-diabetic, and aqueous extract-, oil-, or thymoquinone-treated diabetic rats). Treated rats received 2 mL/kg, i.p., 5%N. sativa extract, 0.2 mL/kg, i.p., N. sativa oil, or 3 mg/mL, i.p., thymoquinone 6 days/week for 30 days. Serum insulin and glucose concentrations, superoxide dismutase (SOD) levels, and pancreatic tissue malondialdehyde (MDA) were determined. Electron microscopy was used to identify any subcellular changes.

RESULTS: Diabetes increased tissue MDA and serum glucose levels and decreased insulin and SOD levels. Treatment of rats with N. sativa extract and oil, as well as thymoquinone, significantly decreased the diabetes-induced increases in tissue MDA and serum glucose and significantly increased serum insulin and tissue SOD. Ultrastructurally, thymoquinone ameliorated most of the toxic effects of STZ, including segregated nucleoli, heterochromatin aggregates (indicating DNA damage), and mitochondrial vacuolization and fragmentation. The aqueous extract of N. sativa also reversed these effects of STZ, but to a lesser extent. The N. sativa oil restored normal insulin levels, but failed to decrease serum glucose concentrations to normal.

CONCLUSIONS: The biochemical and ultrastructural findings suggest that N. sativa extract and thymoquinone have therapeutic and protect against STZ-diabetes by decreasing oxidative stress, thus preserving pancreatic β-cell integrity. The hypoglycemic effect observed could be due to amelioration of β-cell ultrastructure, thus leading to increased insulin levels. Consequently, N. sativa and thymoquinone may prove clinically useful in the treatment of diabetics and in the protection of β-cells against oxidative stress.