Protective effects of Tat-DJ-1 protein against streptozotocin-induced diabetes in a mice model
2018
Yeo, H.J., Hallym University, Chuncheon, Republic of Korea | Yeo, E.J., Hallym University, Chuncheon, Republic of Korea | Shin, M.J., Hallym University, Chuncheon, Republic of Korea | Choi, Y.J., Hallym University, Chuncheon, Republic of Korea | Lee, C.H., Hallym University, Chuncheon, Republic of Korea | Kwon, H.Y., Hallym University, Chuncheon, Republic of Korea | Kim, D.W., Gangneung-Wonju National University, Gangneung, Republic of Korea | Eum, W.S., Hallym University, Chuncheon, Republic of Korea | Choi, S.Y., Hallym University, Chuncheon, Republic of Korea
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.
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