Abstract
Apigenin, a common plant flavonoid, has been extensively studied and showed a wide variety of beneficial effects. The aim of this study was to determine the therapeutic efficacy of starting apigenin treatment 3 day after spinal cord injury (SCI) in rat and to investigate the underlying mechanism. SCI was induced using the modified weight-drop method in Sprague-Dawley rats. The SCI animals were randomly assigned to five groups: sham control group, SCI model group, the methylprednisolone sodium succinate (MPSS) group, the 10 mg/kg apigenin treatment group and the 20 mg/kg apigenin treatment group. First, neuronal function after SCI was evaluated with Basso Beattie Bresnahan locomotor rating scale (BBB) and the result showed that injured animals treated with apigenin showed a significant increase in BBB scores. To explore the underlying mechanism, antioxidative effect of apigenin was assessed by measuring malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities after SCI. Apigenin treatment reversed the decrease of SOD and GSH-Px activity, and the increase of MDA level caused by SCI, suggesting its antioxidative role in response to the injury. In addition, apigenin treatment decreased serum interleukin-1β, tumor necrosis factor-α and intercellular adhesion molecule-1 release after SCI, suggesting an anti-inflammatory effect of apigenin. Finally, apigenin treatment affected the expression level of apoptosis-related gene Bax, Bcl-2 and caspase-3, which indicated its antiapoptosis role after SCI. Our data suggest that apigenin significantly promotes the recovery of rat neuronal function after SCI, which is associated with its antioxidative, anti-inflammatory and antiapoptotic properties.
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