Introduction: The main causes of spinal cord ischemia are a variety of vascular pathologies causing acute arterial occlusions. We investigated neuroprotective effects of coumaric acid on spinal cord ischemia injury in rats.
Methods: Rats were divided randomly into four groups of eight animals as follows: group 1 (control), group 2 (ischemia), group 3 (ischemia+coumaric acid) and group 4 (ischemia+methylprednisolone). In the control group only a laparotomy was performed. In all other groups, the Spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. Levels of malondialdehyde and nuclear respiratory factor 1 were analysed, as were the activitiy of superoxide dismutase. Histopathological and immunohistochemical evaluations were performed. Neurological evaluation was performed with the Tarlov scoring system.
Results: The ischemia+coumaric acid group was compared with the ischemia group, a significant decrease in malondialdehyde and levels was observed (p<0.05). Nuclear respiratory factor 1 level and superoxide dismutase activity of the ischemia+coumaric acid group were significantly higher than ischemia group (p<0.05). In histopathological samples, the ischemia+coumaric acid group is compared with ischemia group, there was a significant increase in numbers of normal neurons (p<0.05). In immunohistochemical staining, hipoxia-inducible factor-1a and NF-kappa B immunopositive neurons were significantly decreased in ischemia+coumaric acid group compared with ischemia group (p<0.05). The neurological deficit scores of ischemia+coumaric acid group were significantly higher than ischemia group at 24 h (p?0.05).
Conclusions: Our results revealed for the first time that coumaric acid exhibits meaningful neuroprotective activity following ischemia-reperfusion injury of the spinal cord.
Patient Care: Further studies based on our findings may be more helpful for investigating this promising medication for SCIR injury.
Learning Objectives: In our study; the anti-oxidant effects of CA have been demonstrated.