کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4299285 | 1288386 | 2016 | 7 صفحه PDF | دانلود رایگان |
BackgroundNeuroinflammatory 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 methodsOne 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.ResultsSCI 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.ConclusionsOur 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.
Journal: Journal of Surgical Research - Volume 203, Issue 2, 15 June 2016, Pages 331–337