Estrogen treatment of spinal cord injury attenuates calpain activation and apoptosis.

Spinal cord injury (SCI) is a devastating neurologic injury, and currently, the only recommended pharmacotherapy is high-dose methylprednisolone, which has limited efficacy. Estrogen is a multi-active steroid with anti-oxidant and anti-apoptotic effects. Estrogen may modulate intracellular Ca2+ and prevent inflammation.

Estrogen attenuated markers of inflammation and decreased lesion volume in acute spinal cord injury in rats.

Spinal cord injury (SCI) is a devastating neurologic injury with functional deficits for which the only currently recommended pharmacotherapy is high-dose methylprednisolone, which has limited efficacy. Estrogen is a multi-active steroid that has shown antiinflammatory and antioxidant effects, and estrogen may modulate intracellular Ca(2+) and attenuate apoptosis. For this study, male rats were divided into three groups.

Higher calpastatin levels correlate with resistance to calpain-mediated proteolysis and neuronal apoptosis in juvenile rats after spinal cord injury.

While the average age for patients admitted with spinal cord injury is 32 years, patients under the age of 16 account for 5% of spinal cord injured persons. For these younger patients, an increased mortality up to 24 h post-injury has been reported, however, survivors may regain more function than their adult counterparts, suggesting that age may play a role in injury tolerance. While the use of growth factors as a therapy for spinal cord injury is well researched, the response of the developing cord to secondary injury has not been thoroughly investigated.

Estrogen as a neuroprotective agent in the treatment of spinal cord injury.

The following review is a brief discussion about spinal cord injury and the possibility of using estrogen as a neuroprotective agent. There are several pathways by which secondary cell death can occur following spinal cord injury, including infiltration of inflammatory cells, generation of reactive oxygen species, decreases in spinal cord blood flow, and increases in intracellular Ca(2+) levels. This secondary damage leads to apoptotic cell death, and the neuroprotective effects of pharmacologic agents have been investigated using experimentally induced spinal cord injury in animals.