It is found that Trigonelline (TG) significantly rescues the morphology of the H9c2 cells. Treatment of cells with Trigonelline attenuates H 2 O 2 induced cell deaths and improves the antioxidant activity. In addition, Trigonelline regulates the apoptotic gene caspase-3, caspase-9 and anti-apoptotic gene Bcl-2, Bcl-XL during H 2 O 2 induced oxidative stress in H9c2 cells. For evident, flow cytometer results also confirms that Trigonelline significantly reduces the H 2 O 2 induced necrosis and apoptosis in H9c2 cells. However, further increment of Trigonelline concentration against H 2 O 2 can induce the necrosis and apoptosis along with H 2 O 2 .
Trigonelline decreases bone mineralization and tends to worsen bone mechanical properties in streptozotocin-induced diabetic rats. In nicotinamide/streptozotocin-treated rats, Trigonelline significantly increases bone mineral density (BMD) and tends to improve cancellous bone strength. Trigonelline differentially affects the skeletal system of rats with streptozotocin-induced metabolic disorders, intensifying the osteoporotic changes in streptozotocin-treated rats and favorably affecting bones in the non-hyperglycemic (nicotinamide/streptozotocin-treated) rats.