Jiang Wu1, Li Maoqiang1, He Fan1, Bian Zhenyu1, He Qifang2, Wang Xuepeng1, Zhu Liulong3. 1. Department of Orthopedics, Nanjing Medical University, Affiliated Hangzhou Hospital (Hangzhou First People's Hospital), Hangzhou, China. 2. Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China. 3. Department of Orthopedics, Nanjing Medical University, Affiliated Hangzhou Hospital (Hangzhou First People's Hospital), Hangzhou, China. Electronic address: drzhuliulong@sina.com.
Abstract
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.
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.