Protective role of berberine and Coptischinensis extract on T2MD rats and associated islet Rin‑5f cells.

The aim of the present study was to compare the different effects of berberine (Ber) and Coptischinensis extract (CCE) on a rat model of type 2 diabetes mellitus (T2DM), and the islet Rin-5f cell line was used to examine the differences between Ber and CCE and the underlying mechanisms. CCE was extracted and purified prior to analysis. Male Sprague-Dawley rats were provided with a high-fat diet to induce insulin resistance prior to injecting with streptozotocinto establish the T2DM model, the T2DM rats were treated with Ber and CCE, and blood samples and pancreatic tissues were obtained and compared to examine T2DM metabolic syndromes among the groups of rats, which included healthy rats, model rats, and model rats treated with Ber and CCE at different doses between 0 and 8 weeks. The protective effects of Ber and CCE on the Rin-5f islet cell line were also evaluated. The effects on Rin-5f cell proliferation and cell cycle, glucose-stimulated insulin release test (GSIS), the anti-apoptotic effects caused by fat induction, and protein expression levels of poly ADP-ribose polymerase (PARP-1) were evaluated. The results showed that the content of the prepared CCE was 96.07% for five alkaloids. When it was used for treatment of the T2DM rats, compared with Ber, metformin and rosiglitazone, the fasting blood glucose, glucosylated serum protein (GSP) and glucose infusion rate indicesin the fasting rats were ameliorated, compared with those in the T2MD rats, with no significant differences between treatment with Ber or CCE and metformin or rosiglitazone. The indices of mean optical density and fasting beta-cell function index (FBCI) were different following treatment with Ber and CCE, compared with those in the model rats, which may have stimulated the pancreatic secretion of insulin. When Ber and CCE were used to examine the protective effects on Rin-5F cells, it was found that the Rin-5f cell GSIS, cell cycle, lipotoxic islet cell proliferation and protein expression of PARP-1 were altered and improved, which may have protected pancreatic islet beta-cells by improving islet beta-cell proliferation and the protein expression of PARP-1. CCE and Ber exerted similar effects when used for the treatment of T2MD rats, and may have stimulated the pancreatic secretion of insulin through the protective effect on islet beta-cells via improving islet beta-cell proliferation and the protein expression of PARP-1.