Protection of Curcumin against Streptozocin-Induced Pancreatic Cell Destruction in T2D Rats.

Abstract

As a kind of traditional Chinese medicine extract, curcumin has been proven to be effective in inhibiting inflammation and apoptosis in pancreatic islet β cells in the streptozotocin-induced diabetes mellitus rat model, although the underlying mechanism has not yet been clarified. To examine the effect of curcumin on inflammation and apoptosis in pancreatic islet β cells, we established a type 2 diabetes rat model by feeding the animals a high-fat diet and intraperitoneally injecting streptozotocin. The curcumin was administered by intraperitoneal injection. The rat body weight, fasting blood glucose, intraperitoneal glucose tolerance tests, and insulin tolerance tests were recorded and analyzed. Hematoxylin and eosin staining was used for morphological analysis, and a TUNEL assay was performed to detect the apoptotic cells. The expression levels of proteins related to oxidative stress, inflammation and apoptosis were detected by Western blotting and ELISA. Curcumin administration significantly decreased fasting blood glucose and promoted recovery of pancreas function in type 2 diabetes rats. In curcumin-treated rats, the pancreatic tissue destruction and apoptosis index were reduced. The expression of IL-1β, IL-6, TNF-α, caspase-3, Bax, and malondialdehyde were significantly reduced, and Bcl-2, superoxide dismutase 2, and glutathione peroxidase were significantly increased. Curcumin inhibited the expression of phosphorylated JNK and NF-κB proteins to block the RAGE/JNK/NF-κB signaling pathway. In conclusion, these results indicate that curcumin blocks the phosphorylation of JNK and NF-κB protein to inhibit this signaling pathway, thereby further inhibiting inflammation and apoptosis in pancreatic islet β cells. Curcumin has potential value for the treatment of diabetes.