Curcumin prevents streptozotocin-induced islet damage by scavenging free radicals: a prophylactic and protective role.

Pancreatic islet cell death is the cause of deficient insulin production in diabetes mellitus. Approaches towards prevention of cell death are of prophylactic importance in control and management of hyperglycemia. Generation of oxidative stress is implicated in streptozotocin, a beta cell specific toxin-induced islet cell death. In this context, antioxidants raise an interest for therapeutic purposes. Curcumin, a common dietary spice is a well known antioxidant and hence we investigated its effect on streptozotocin-induced islet damage in vitro. Isolated islets from C57/BL6J mice were incubated with curcumin for 24 h and later exposed to streptozotocin for 8 h. The effect of streptozotocin exposure to islets was determined with respect to islet viability and functionality, cellular reactive oxygen species concentrations and levels of activated poly (ADP-ribose) polymerase-1. Cellular antioxidant potential (Cu/Zn superoxide dismutase) and advanced glycation end-product related damage was assessed to determine the metabolic status of treated and untreated islets. Islet viability and secreted insulin in curcumin pretreated islets were significantly higher than islets exposed to streptozotocin alone. Curcumin retarded generation of islet reactive oxygen species along with inhibition of Poly ADP-ribose polymerase-1 activation. Although curcumin did not cause overexpression of Cu/Zn superoxide dismutase, it prevented reduction in levels of cellular free radical scavenging enzymes. Our data shows that curcumin protects islets against streptozotocin-induced oxidative stress by scavenging free radicals. We show here for the first time, that prophylactic use of curcumin may effectively rescue islets from damage without affecting the normal function of these cellular structures.