Wu Jiang, Maoqiang Li, Fan He, Zhenyu Bian, Qifang He, Xuepeng Wang, Liulong Zhu
Department of Orthopedics, Nanjing Medical University, Affiliated Hangzhou Hospital (Hangzhou First People's Hospital), Hangzhou, China.
Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
J Surg Res. 2016 Jun 15;203(2):331-7. doi: 10.1016/j.jss.2016.02.041. Epub 2016 Mar 5.
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).
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.
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.
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.
神经炎症反应涉及白细胞介素(IL)-1β和IL-18的激活。促炎IL的加工和激活需要NLRP3炎性小体的激活。芦丁可以保护脊髓免受损伤,但其潜在机制尚不清楚。在此,我们研究了芦丁介导的脊髓损伤(SCI)大鼠模型神经保护作用的分子机制。
120只雌性Sprague-Dawley大鼠随机分为四组:假手术组、SCI组、SCI + 芦丁50组和SCI + 芦丁100组。分析芦丁对炎症标志物水平、组织学改变和运动评分的影响。
SCI显著增加了NLRP3、ASC、IL-1β、IL-18和肿瘤坏死因子-α的表达。芦丁显著降低了活性氧、丙二醛、NLRP3、ASC、半胱天冬酶-1、IL-1β、IL-18和肿瘤坏死因子-α的水平。此外,给予芦丁显著减轻了组织学改变并改善了运动恢复。
我们的数据提供了明确的证据,表明芦丁可减轻组织损伤并改善运动恢复,其机制可能与减轻炎症和氧化应激有关。