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We appreciate the interest in our research1 and could not agree more with the authors of this comment. The purpose of our teaching neuroimage was to point out that not only radiographic appearances of a herniated lumbar disc (HLD) could potentially mimic a spinal tumor but that the clinical presentation of a HLD could mimic a spinal tumor as well.1

A 47-year-old healthy man presented with intermittent low back pain radiating to the left calf; within 1 month, the pain worsened at night and disturbed his sleep. Examination showed paresthesia in left lateral calf, weakness in left ankle plantarflexion, and decreased ankle reflex. Neuroimaging revealed near-total obliteration of the spinal canal by a 2 × 1.2 cm nodule at L5-S1 level with ring enhancement under gadolinium-enhanced MRI (figure 1). The patient underwent surgery for a presumed spinal tumor. The intraoperative and pathologic findings revealed ruptured intervertebral disc without neoplasm (figure 2). The clinical presentation and image characteristics of a large ruptured disc can mimic a spinal tumor.1,2

We explored anti-inflammatory potential of melatonin against the lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro. RAW 264.7 and BV2 cells were stimulated by LPS, followed by the treatment with melatonin or vehicle at various time intervals. In a mouse model of meningitis induced by LPS, melatonin (5 mg/kg) or vehicle was intravenously injected at 30 min postinsult. The activity of matrix metalloproteinase-2 (MMP-2) and metalloproteinase-9 (MMP-9) was determined by gelatin zymography. Nuclear factor-kappa B (NFκB) translocation and binding activity were determined by immunocytochemistry and electrophoretic mobility shift assay (EMSA). Our results showed that either pretreatment or cotreatment with melatonin at 50–500 μm effectively inhibited the LPS-induced proMMP-9 activation in the RAW 264.7 and BV2 cells, respectively (P

We have shown that administration of Cinnamophilin (CINN) effectively reduced oxidative damage, DNA lipid peroxidation, neutrophil infiltration, and ischemic brain damage by inhibiting oxidative stress and the resulting inflammation in experimental stroke. In this study the potential CINN to ameliorate neutrophilic respiratory burst and reduce neutrophil infiltration was investigated. Neutrophils pretreated or co-treated with CINN, were stimulated by phorbol 12-myristate 13-acetate (PMA) and the levels of superoxide radical (O2-.) and hydrogen peroxide (H2O2) produced were determined by dihydroethidium (DHE) and dihydrorhodamine-123 (DHR) fluorescence assays, respectively, while myeloperoxidase activity (MPO) was measured by the guaiacol method. Our results showed that both pretreatment and co-treatment with CINN significantly inhibited H2O2 production in PMA-stimulated neutrophils. Additionally, cotreatment, but not pretreatment, with CINN effectively inhibited O2-. production in the PMA-stimulated neutrophils. Both treatments did not effectively reduce the MPO activity in neutrophil. Finally, animals treated with CINN at reperfusion brain insults significantly reduced brain infarction and neutrophil infiltration, as well as improved neurobehavioral outcome following cerebral ischemic reperfusion. These results support pluripotent neuroprotection actions offered by CINN against cerebral ischemia-reperfusion.

We explored anti-inflammatory potential of melatonin against the lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro. RAW 264.7 and BV2 cells were stimulated by LPS, followed by the treatment with melatonin or vehicle at various time intervals. In a mouse model of meningitis induced by LPS, melatonin (5mg/kg) or vehicle was intravenously injected at 30min postinsult. The activity of matrix metalloproteinase-2 (MMP-2) and metalloproteinase-9 (MMP-9) was determined by gelatin zymography. Nuclear factor-kappa B (NFκB) translocation and binding activity were determined by immunocytochemistry and electrophoretic mobility shift assay (EMSA). Our results showed that either pretreatment or cotreatment with melatonin at 50-500 μm effectively inhibited the LPS-induced proMMP-9 activation in the RAW 264.7 and BV2 cells, respectively (P0.05). This melatonin-induced proMMP-9 inhibition remained effective when treatment was delayed up to 2 and 6hr postinsult for RAW 264.7 and BV2 cells, respectively (P0.05 for both groups). Additionally, melatonin significantly attenuated the rises of circulatory and cerebral MMP-9 activity, respectively (P0.05) and reduced the loss of body weight (P0.05) in mice with meningitis. Moreover, melatonin (50μm) effectively inhibited nuclear factor-kappa B (NFκB) translocation and binding activity in the LPS-treated RAW 264.7 and BV2 cells, respectively (P0.05). These results demonstrate direct inhibitory actions of melatonin against postinflammatory NFκB translocation and MMP-9 activation and highlight its ability to inhibit systemic and cerebral MMP-9 activation following brain inflammation.