Background: Neuroinflammatory responses involve the activation of the interleukin (IL) -1β and IL-18. Processing and activation of the pro-inflammatory IL require NLRP3 inflammasome activation. Rutin can protect spinal cord against damage, but the potential mechanisms underlying remain unknown. Here, we investigated the molecular mechanisms of rutin-mediated neuroprotection in a rat model of spinal cord injury (SCI).
Materials and methods: One hundred twenty female Sprague-Dawley rats were randomly assigned to four groups: sham group, SCI group, SCI + Rutin50 group, and the SCI + Rutin100 group. The influences of rutin on inflammatory marker levels, histologic alterations, and locomotion scale were analyzed.
Results: SCI significantly increased the expression of the NLRP3, ASC, IL-1β, IL-18, and tumor necrosis factor-alpha. Rutin significantly reduced the levels of reactive oxygen species, malondialdehyde, NLRP3, ASC, caspase-1, IL-1β, IL-18, and tumor necrosis factor-alpha. Furthermore, rutin administration significantly attenuated histologic alteration and improved locomotion recovery.
Conclusions: Our data provide clear evidence that rutin attenuates tissue damage and improves locomotion recovery, and the mechanism may be related to the alleviation of inflammation and oxidative stress.
Keywords: Inflammation; NLRP3 inflammasome; Reactive oxygen species; Rutin; Spinal cord injury.
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