The role of neuroprotective and antioxidant effects in reducing motor dysfunction, mechanical allodynia and heat hyperalgesia caused by spinal cord injury in rats following intrathecal administration of metformin

Spinal cord injury (SCI) is a debilitating sensory-motor dysfunction. Neuropathic pain and motor dysfunction are the most common types of dysfunctionality after SCI, which reduces the quality of life. So far, SCI treatment has not been completely effective and researchers are seeking for novel alternative/potent therapies. Metformin has shown antioxidant and anti-inflammatory effects on the central and peripheral nervous systems. In the present study, the probable neuroprotective and antioxidant effects of intrathecal metformin administration was evaluated on the neuropathic pain and motor dysfunction after SCI.

Thirty-five rats were divided into five groups: sham, SCI, and metformin (Met) at doses of 1, 2 and 4 mM. Hot plate, acetone, and von Frey behavioral tests and weight changes were performed on days 7, 14, 21, and 28 after SCI. The changes in serum levels of catalase and glutathione, as well as nitrite level, and numbers of sensory and motor neurons were measured on day 28 after surgery.

Intrathecal injection of metformin reduced heat, cold and mechanical pain, motor activity, and modulated weight changes in rats after SCI. Intrathecal metformin also attenuated serum changes of catalase and glutathione, decreased serum nitrite, and increased survived sensory and motor neurons after SCI.

Employing the neuroprotective and antioxidant potential of intrathecal metformin administration could reduce neuropathic pain and improve motor dysfunction following SCI.
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