Trigonelline inhibits caspase 3 to protect β cells apoptosis in streptozotocin-induced type 1 diabetic mice

As a main active ingredient of Fenugreek, trigonelline has protective efficiency on type 2 diabetes and diabetic peripheral neuropathy in rats. This study investigates the protection of trigonelline on hyperglycemia, beta cell apoptosis, and inflammation in type 1 diabetic mice. Streptozotocin (160 mg/kg) was intraperitoneal injected to induce diabetic mice. There were 4 groups: normal control, diabetes, trigonelline-treated diabetes, and insulin-treated diabetes. After 4-week treatment, levels of blood glucose, serum insulin, and inflammatory factors-beta cell apoptosis, insulin content, and oxidative stress parameters in pancreas were calculated. Pancreas was examined by immunohistochemistry staining and hematoxylin/eosin. Trigonelline significantly declined the levels of blood glucose, serum tumor necrosis factor-alpha, interleukin-6, and interleukin-1 beta, while increased the levels of serum insulin and adiponectin in diabetic mice. Insulin content, glutathione concentration, serum activities of super-oxide dismutase and catalase in pancreas, and pancreas to body weight ratio were remarkably decreased, while serum malondialdehyde concentration was increased in diabetic mice. Trigonelline treatment restored the above mentioned parameters. Trigonelline even suppresses beta cell apoptosis via downregulating caspase 3 expression. These results imply that trigonelline protects diabetic mice mediated by decreasing blood glucose, increasing insulin expression in beta cells, regulating inflammatory response, suppressing beta cells apoptosis partly by down-regulating caspase 3 expression, and raising antioxidant enzyme activity.