Vanillin ameliorates changes in HIF-1α expression and neuronal apoptosis in a rat model of spinal cord injury.

Abstract

In the search for treating neurological dysfunctions after spinal cord injury (SCI), methods of neuroprotection are of interest to intervene with the caspase pathway. To evaluate the neuroprotective effects of vanillin in a rat model of spinal cord injury (SCI). Rats were randomly assigned to one of three groups: a sham-operated group, and two groups where SCI was produced by ischemia/reperfusion which received either saline or vanillin (286 mg/kg, intraperitoneal [i.p.] 30 min prior to surgery). Neurological function was estimated by the Tarlov scale at 1, 12, and 24 h after surgery. Additionally, we estimated the levels of oxidative stress, inflammatory cytokines, and mitochondrial proteins in the homogenates of spinal tissues and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and immunohistochemical assays of spinal tissues. Motor dysfunction was found to be significantly improved in the vanillin treated group compared to SCI rats. This was accompanied by altered levels of oxidative stress, inflammatory cytokines, and expressions of mitochondrial proteins in the SCI rats which were ameliorated by the vanillin treatment. Vanillin also significantly reduced the number of TUNEL-positive cells in spinal cord tissues compared to the sham group (p < 0.01) and decreased the number of hypoxia-inducible factor (HIF)-1α-positive cells. In the SCI rat model vanillin exerted neuroprotective effects of reducing apoptosis and attenuating the expression of HIF-1α in spinal tissues.