Effect of humic acid on oxidative stress and neuroprotection in traumatic spinal cord injury: an experimental study.

BACKGROUND/AIM: Traumatic spinal cord injury (TSCI) is an important health problem, especially in developing countries with additional socioeconomic loss. Humic acid (HA) usually has antioxidant, antiinflammatory, blood circulating, and antiviral effects. Hence, it was aimed herein to show the effect of HA on neuroprotection in a TSCI model.

MATERIALS AND METHOD

A TSCI model was used, in which 24 Wistar albino rats were divided into 4 groups: control group: subjected to only laminectomy; sham group: subjected to laminectomy + TSCI; HA 5 mg/kg group: subjected to laminectomy + TSCI + intraperitoneal (IP) injection of 5 mg/kg of HA; and HA 10 mg/kg group: subjected to laminectomy + TSCI + IP injection of 10 mg/kg of HA. Intracardiac blood samples were obtained preoperatively (preop), and at 1 and 24 h postoperatively (postop). The total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels were evaluated in the serum. The motor functions were evaluated using the Modified Tarlov Score at 24 h postop.

RESULTS

There were no significant changes in the TAS values between the sham and HA 5 mg/kg and HA 10 mg/kg groups (p = 0.77/0.21). However there was a significant decrease in the TOS values at 24 h postop when comparing the sham and HA 5 mg/kg groups (p = 0.02). The pathological evaluation showed a significant decrease in the severity of edema, hemorrhage, polymorphonuclear leucocyte (PNL) infiltration, and mononuclear leucocyte (MNL)/macrophage/microglia infiltration when compared with the control group (p < 0.05). There was a significant recovery at the paraplegia level when the HA 5 mg/kg and HA 10 mg/kg groups were compared with the control group (p < 0.001).

CONCLUSION

The effects of HA in the early stages of TSCI on oxidative stress, histopathological changes, and neurological improvement were investigated herein. It is thought to be a potential therapeutic agent in acute TSCI but needs to be further evaluated to determine the extent of its effect on other neuroprotective pathways in larger series.