Acute administration of tibolone reduces oxidative stress and inflammation in a rat model of traumatic spinal cord injury.

BACKGROUND

As a complex condition, spinal cord injury (SCI) has devastating consequences for physical, financial, social, and emotional well-being. After SCI, damage increases due to oxidative stress (OS) and inflammation, mechanisms which have been identified as potential therapeutic targets. Tibolone (TIB), a selective tissue estrogen activity regulator (STEAR), has neuroprotective properties demonstrated in some experimental models.

OBJECTIVE

We investigated the effect of TIB on OS and inflammation in a rat model of traumatic SCI.

Methods

Moderate contusion SCI was produced at thoracic level 9 (T9) in male Sprague Dawley rats. The animals were then divided into groups and received oral doses of TIB (0.1, 1, and 10 mg/kg) at various times (30 minutes, 24, and 48 hours). Animals underwent euthanasia 72 hours after the SCI. Spinal cord tissue and serum samples were collected for the analysis of OS (superoxide dismutase activity (SOD), malondialdehyde (MDA) levels, and protein carbonyl concentration), and inflammation markers (IL-6, IL-1β, and TNFα concentration).

RESULTS

TIB administration significantly increased SOD activity in the spinal cord tissue but not in the serum. In contrast, TIB decreased MDA and carbonyl levels in both samples. Also, TIB decreased pro-inflammatory cytokine levels (IL-6, IL-1β, and TNFα) in the spinal cord tissue and serum.

CONCLUSIONS

The best results were observed with the 0.1 mg/kg dose. TIB demonstrated a protective effect by decreasing OS and inflammation after SCI, suggesting an estrogenic effect of this STEAR. However, further studies should be conducted to elucidate the exact mechanism by which TIB exerts neuroprotection after SCI.