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7,8-Dihydroxyflavone Protects High Glucose-Damaged Neuronal Cells against Oxidative Stress

  • Cho, Suk Ju (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Kang, Kyoung Ah (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Piao, Mei Jing (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Ryu, Yea Seong (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Fernando, Pincha Devage Sameera Madushan (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Zhen, Ao Xuan (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Hyun, Yu Jae (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Ahn, Mee Jung (Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University) ;
  • Kang, Hee Kyoung (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine) ;
  • Hyun, Jin Won (Jeju National University School of Medicine and Jeju Research Center for Natural Medicine)
  • Received : 2018.10.16
  • Accepted : 2018.11.06
  • Published : 2019.01.01

Abstract

Oxidative stress is considered a major contributor in the pathogenesis of diabetic neuropathy and in diabetes complications, such as nephropathy and cardiovascular diseases. Diabetic neuropathy, which is the most frequent complications of diabetes, affect sensory, motor, and autonomic nerves. This study aimed to investigate whether 7,8-dihydroxyflavone (7,8-DHF) protects SH-SY5Y neuronal cells against high glucose-induced toxicity. In the current study, we found that diabetic patients exhibited higher lipid peroxidation caused by oxidative stress than healthy subjects. 7,8-DHF exhibits superoxide anion and hydroxyl radical scavenging activities. High glucose-induced toxicity severely damaged SH-SY5Y neuronal cells, causing mitochondrial depolarization; however, 7,8-DHF recovered mitochondrial polarization. Furthermore, 7,8-DHF effectively modulated the expression of pro-apoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) under high glucose, thus inhibiting the activation of caspase signaling pathways. These results indicate that 7,8-DHF has antioxidant effects and protects cells from apoptotic cell death induced by high glucose. Thus, 7,8-DHF may be developed into a promising candidate for the treatment of diabetic neuropathy.

Keywords

References

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