Abstract
Sulforaphane (SFP) treatment represses oxidative stress by activating NRF2. Meanwhile, SFP may also increase the production of nitric oxide (NO) and activate the signaling pathway of cyclic guanosine monophosphate (cGMP), which is involved in the pathogenesis of hypoxic vestibular vertigo (HVV). However, it remains unknown as whether SFP plays a therapeutic role in the treatment of HVV. A rat model of HVV was established to measure the levels of escape latency, malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) in the aorta tissues. Quantitative real-time PCR was performed to evaluate the expression of NRF2 mRNA, and Western blot and immunohistochemistry were carried out to analyze the expression of NRF2 protein. ELISA was used to examine the production of NO and cGMP. SFP treatment helped to maintain the escape latency and MDA, GSH, SOD concentrations in the brain of HVV rats, and recovered the expression of NRF2 inhibited in the brain of HVV rats. SFP treatment also elevated NO and cGMP production that was down-regulated in the brain of HVV rats. On the cellular level, SFP enhanced the expression of NRF2, reduced the concentrations of MDA, GSH and SOD, and promoted the production of NO and cGMP in a dose-dependent manner. In this study, we treated an animal model of HVV with SFP to investigate its effect on NO production and oxidative stress. Our work provided a mechanistic insight into the therapeutic effect of SFP on the treatment of HVV.
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