Curcumin possesses medicinal properties that are beneficial in various diseases, such as heart disease, cancer, and type 2 diabetes mellitus (T2 DM). It has been proposed that pancreatic beta cell dysfunction in T2 DM is promoted by oxidative stress caused by NADPH oxidase over-activity. The aim of the present study was to evaluate the efficacy of curcumin as a protective agent against high glucose/palmitate (HP)-induced islet cell damage and in streptozotocin (STZ)-induced DM rats. INS-1 cells were exposed to HP with or without curcumin. Cell proliferation, islet cell morphological changes, reactive oxygen species production, superoxide dismutase and catalase activity, insulin levels, NADPH oxidase subunit expression, and the expression of apoptotic factors by INS-1 cells were observed. Our results show that curcumin can effectively inhibit the impairment of cell proliferation and activated oxidative stress, increase insulin levels, and reduce the high expression of NADPH oxidase subunits and apoptotic factors induced by HP in INS-1 cells. The STZ-induced DM rat model was also used to determine whether curcumin can protect islets in vivo. Our results show that curcumin significantly reduced pathological damage and increased insulin levels of islets in STZ-induced DM rats. Curcumin also successfully inhibited the high expression of NADPH oxidase subunits and apoptotic factors in STZ-induced DM rats. These results suggest that curcumin is able to attenuate HP-induced oxidative stress in islet cells and protect these cells from apoptosis by modulating the NADPH pathway. In view of its efficiency, curcumin has potential for translation applications in protecting islets from glucolipotoxicity.

姜黄素具有对多种疾病有益的药用特性，例如心脏病，癌症和2型糖尿病（T2 DM）。已经提出，由NADPH氧化酶过度活性引起的氧化应激可促进T2 DM中的胰腺β细胞功能障碍。本研究的目的是评估姜黄素作为抗高葡萄糖/棕榈酸（HP）诱导的胰岛细胞损伤和链脲佐菌素（STZ）诱导的DM大鼠的保护剂的功效。在有或没有姜黄素的情况下，将INS-1细胞暴露于HP。观察到INS-1细胞的细胞增殖，胰岛细胞形态变化，活性氧产生，超氧化物歧化酶和过氧化氢酶活性，胰岛素水平，NADPH氧化酶亚基表达以及凋亡因子的表达。我们的结果表明姜黄素可有效抑制INS-1细胞中细胞增殖的损伤和激活的氧化应激，增加胰岛素水平，并减少HP诱导的NADPH氧化酶亚基和凋亡因子的高表达。STZ诱导的DM大鼠模型也用于确定姜黄素是否可以保护胰岛体内。我们的结果表明，姜黄素可显着降低STZ诱导的DM大鼠的病理损伤和胰岛胰岛素水平的升高。姜黄素还可以成功抑制STZ诱导的DM大鼠中NADPH氧化酶亚基和凋亡因子的高表达。这些结果表明姜黄素能够减轻胰岛细胞中HP诱导的氧化应激，并通过调节NADPH途径保护这些细胞免于凋亡。鉴于其效率，姜黄素具有翻译应用潜力，可保护胰岛免受糖脂毒性。