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Keigyou Yoh^1,, Aki Hirayama^2,, Kazusa Ishizaki³, Akiko Yamada³, Masayoshi Takeuchi⁴, Sho-ichi Yamagishi⁵, Naoki Morito¹, Takako Nakano³, Masami Ojima³, Homare Shimohata¹, Ken Itoh⁶, Satoru Takahashi^3,* and Masayuki Yamamoto⁷

¹ Pathophysiology of Renal Diseases, Doctoral Program in Clinical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 305-8575, Japan
² Center for Integrative Medicine, Tsukuba University of Technology, Tsukuba 305-8521, Japan
³ Anatomy and Embryology, Doctoral Program in Life System Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 305-8575, Japan
⁴ Department of Pathophysiological Science, Faculty of Pharmaceutical Science, Hokuriku University, Kanazawa 920-1181, Japan
⁵ Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan
⁶ Department of Stress Response Science, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
⁷ Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan

The transcription factor Nrf2 regulates the expression of antioxidant genes. Hyperglycemia-induced oxidative stress is involved in the pathogenesis of diabetes and its complications. However, little is known about the protective role of Nrf2 in diabetes. To gain insight into the protective role of Nrf2 in diabetes we treated Nrf2 knockout (Nrf2 KO) mice with streptozotocin (STZ). The STZ Nrf2 KO mice did not develop renal hyperfiltration, which was observed in the STZ-treated wild-type (STZ WT) mice, but renal function gradually deteriorated over the 10-week observation period. Urinary excretion of nitric oxide metabolites and the occurrence of 8-nitroguanosine, which was detected in glomerular lesions, were increased in STZ Nrf2 KO mice during the early stages after treatment. In vivo electron paramagnetic resonance analysis revealed an accelerated rate of decay of the 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl spin probe signal in STZ Nrf2 KO mice. The addition of superoxide dismutase prolonged the half-life of the signal, which suggested that increased oxygen radical formation occurred in the STZ Nrf2 KO mice. These results suggested that hyperglycemia increased oxidative and nitrosative stress and accelerated renal injury in the Nrf2 KO mice and that Nrf2 serves as a defense factor against some diabetic complications.

These authors contributed equally to this work.

^* Correspondence: satoruta{at}md.tsukuba.ac.jp

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