Tat-HSP70 protects neurons from oxidative damage in the NSC34 cells and ischemic damage in the ventral horn of rabbit spinal cord

• Published in: Neurochemistry international Vol. 129; p. 104477
• Main Authors: Kim, Woosuk, Kwon, Hyun Jung, Jung, Hyo Young, Yoo, Dae Young, Moon, Seung Myung, Kim, Dae Won, Hwang, In Koo
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.10.2019
• Subjects: Heat shock protein 70; Neuroprotection; Oxidative stress; Rabbit; Spinal cord ischemia; Spinal cord ischemia; Rabbit; Oxidative stress; Neuroprotection; Heat shock protein 70
• ISSN: 0197-0186; 1872-9754
• DOI: 10.1016/j.neuint.2019.104477

Heat shock protein 70 (HSP70) is an ATP-dependent molecular chaperone, and it has been shown that its levels increase after exposure to various types of stress, including ischemia. In the present study, we investigated the effects of HSP70 against H2O2-induced neuronal stress in NSC34 cells and against spinal cord ischemia in rabbits. Tat-HSP70 proteins facilitated the intracellular delivery of HSP70 into the NSC34 cells and enabled them to cross the blood-brain barrier in the rabbit spinal cord. Tat-HSP70 was effectively transduced into NSC34 cells in a concentration- and time-dependent manner, while control-HSP70 protein could not be delivered intracellularly at any concentration or time after treatment. Treatment with Tat-HSP70 reduced the generation of reactive oxygen species and cell death induced by H2O2, while the control-HSP70 did not show any significant effect on the NSC34 cells exposed to H2O2. In rabbit spinal cord, the administration of Tat-HSP70 showed significant amelioration of neurological defects and neuronal death in the ventral horn of spinal cord. In addition, Tat-HSP70 treatment significantly reduced lipid peroxidation and increased Cu, Zn-superoxide dismutase activities in the spinal cord, but glutathione peroxidase and Mn-superoxide dismutase activities remained unchanged. These results suggest that Tat-HSP70, not control-HSP70, decreases cell damage by reducing oxidative stress in NSC34 cells and rabbit spinal cord, and it can be employed for the reduction of neuronal damage caused after spinal cord ischemia. •Tat-HSP70 enables to efficiently transduce into the NSC34 cells.•Tat-HSP70 reduces the H2O2-induced neuronal death and oxidative damage in the NSC34 cells.•Tat-HSP70 protects motor neurons from spinal cord ischemia by reducing the lipid peroxidation.