Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
BMB Rep. 2018 Jul;51(7):362-367. doi: 10.5483/bmbrep.2018.51.7.101.
A major feature of type 1 diabetes mellitus (T1DM) is hyperglycemia and dysfunction of pancreatic β-cells. In a previous study, we have shown that Tat-DJ-1 protein inhibits pancreatic RINm5F β-cell death caused by oxidative stress. In this study, we examined effects of Tat-DJ-1 protein on streptozotocin (STZ)-induced diabetic mice. Wild type (WT) Tat-DJ-1 protein transduced into pancreas where it markedly inhibited pancreatic β-cell destruction and regulated levels of serum parameters including insulin, alkaline phosphatase (ALP), and free fatty acid (FFA) secretion. In addition, transduced WT Tat-DJ-1 protein significantly inhibited the activation of NF-κB and MAPK (ERK and p38) expression as well as expression of COX-2 and iNOS in STZ exposed pancreas. In contrast, treatment with C106A mutant Tat-DJ-1 protein showed no protective effects. Collectively, our results indicate that WT Tat-DJ-1 protein can significantly ameliorate pancreatic tissues in STZ-induced diabetes in mice. [BMB Reports 2018; 51(7): 362-367].
1 型糖尿病的一个主要特征是高血糖和胰腺β细胞功能障碍。在之前的研究中，我们已经表明 Tat-DJ-1 蛋白抑制氧化应激引起的胰岛 RINm5F β细胞死亡。在这项研究中，我们检查了 Tat-DJ-1 蛋白对链脲佐菌素（STZ）诱导的糖尿病小鼠的影响。野生型（WT）Tat-DJ-1 蛋白转导到胰腺中，明显抑制了胰腺β细胞的破坏，并调节了包括胰岛素、碱性磷酸酶（ALP）和游离脂肪酸（FFA）分泌在内的血清参数水平。此外，转导的 WT Tat-DJ-1 蛋白显著抑制了 NF-κB 和 MAPK（ERK 和 p38）表达以及 COX-2 和 iNOS 在 STZ 暴露胰腺中的表达的激活。相比之下，用 C106A 突变 Tat-DJ-1 蛋白处理则没有保护作用。总之，我们的结果表明，WT Tat-DJ-1 蛋白可以显著改善 STZ 诱导的糖尿病小鼠的胰腺组织。[BMB 报告 2018；51(7): 362-367]。
