Therapeutic effect of apocynin through antioxidant activity and suppression of apoptosis and inflammation after spinal cord injury.
Exp Ther Med. 2017 Mar ;13(3):952-960. Epub 2017 Jan 25. PMID: 28450925
Spinal cord injury (SCI) is a devastating condition affecting hundreds of thousands of people worldwide annually. SCI results in activation of the inflammatory response and apoptosis, and generates oxidative stress, which has deleterious effects on the recovery of motor function. Apocynin, an inhibitor of NADPH oxidase, has been demonstrated to improve neuronal functional recovery in rat models of SCI. However, the efficacy of apocynin treatment post-SCI has not been investigated. The aim of this study was to observe the effects of apocynin on the repair of acute spinal cord damage in rats and to examine the potential beneficial effects. A rat model of SCI was established, and apocynin (50 mg/kg) was administered intraperitoneally at 30 min after SCI and then every 12 h for 3 days. In order to examine oxidative tissue injury, the levels of malondialdehyde and glutathione and activities of myeloperoxidase and superoxide dismutase in the spinal cord tissues were measured. Histological evaluations were also conducted. NeuN labeling, TUNEL staining and caspase 3 immunohistochemical staining were performed to analyze neuronal damage and apoptosis around the lesion. Immunohistochemical analysis was also carried out to observe the expression of CD11b and glial fibrillary acidic protein. The expression levels of bax, bcl-2, tumor necrosis-α, interleukin (IL)-1β and IL-6 in the spinal cord tissue were assayed by western blotting. Finally, locomotor function was evaluated using the inclined plane test and Basso, Beattie and Bresnahan scores. The results showed that treatment with apocynin decreased oxidative damage, alleviated neuronal apoptosis, inhibited the inflammatory response and resulted in the promotion of locomotor function. Therefore, this study confirmed the therapeutic efficacy of apocynin in the repair of SCI, which was probably mediated via the inhibition of apoptosis and the inflammatory response, thus promotingthe restoration of nerve function.