摘要
目的:探讨白藜芦醇抗小鼠炎性痛的核因子κB(nuclear factor-κB,NF-κB)信号通路机制。方法:将60只BALB/c小鼠随机分为正常对照组、炎性痛模型组、阳性对照(地塞米松,0.5 mg/kg)组及白藜芦醇(100、50和25 mg/kg)组,每组10只。通过测定小鼠机械刺激缩足反射阈值、热刺激缩足反应潜伏期及冷缩足反射次数,观察白藜芦醇是否具有缓解小鼠炎性痛的作用。采用RT-PCR和Western blot法检测炎性痛小鼠脊髓组织(L4~L6)NF-κB、NF-κB抑制蛋白α(inhibitor of NF-κBα,IκBα)、NF-κB抑制蛋白激酶β(inhibitor of NF-κB kinaseβ,IKKβ)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)及白细胞介素1β(interleukin-1β,IL-1β)的mRNA和蛋白表达水平的影响。结果:白藜芦醇(100和50 mg/kg)可明显升高完全弗氏佐剂(complete Freund’s adjuvant,CFA)所致炎性痛小鼠机械刺激缩足反射阈值,显著延长其热刺激缩足反应潜伏期,减少其冷缩足反射次数(P<0.05或P<0.01);白藜芦醇(100 mg/kg)可明显下调CFA诱导的炎性痛小鼠脊髓组织NF-κB、IκBα、IKKβ、TNF-α及IL-1β的mRNA和蛋白表达水平(P<0.05或P<0.01)。结论:白藜芦醇对炎性痛具有较好的缓解作用,其机制可能与抑制NF-κB信号通路有关。
AIM: To investigate the anti-inflammatory action of resveratrol( Res) and its correlation with nuclear factor-κB( NF-κB) signaling pathway in a mouse model of inflammatory pain. METHODS: BALB/c mice( n = 60)were randomly divided into 6 groups: normal control group,inflammatory pain model group,positive control( dexamethasone,0. 5 mg/kg) group and resveratrol( 100,50 and 25 mg/kg) groups( 10 mice in each group). In order to observe the anti-inflammatory pain effects of reseratrol on mice,the paw withdrawal mechanical threshold,paw withdrawal thermal latency and cold withdrawal times were detected. In order to analyze the mechanism of analgesic effect of resveratrol,the expression levels of NF-κB,inhibitor of NF-κB( IκB) α,inhibitor of NF-κB kinase( IKK) β,tumor necrosis factor( TNF)-α and interleukin( IL)-1β in the spinal cord tissues( L4 ~ L6) of the mice were determined by RT-PCR and Western blot. RESULTS: The resveratrol at 100 and 50 mg/kg increased the paw withdrawal mechanical threshold,prolonged the paw withdrawal thermal latency,and decreased the cold withdrawal times in the inflammatory pain mice( P 〈0. 05 or P 〈 0. 01). The resveratrol at 100 mg/kg down-regulated the mRNA and protein expression levels of NF-κB,IκBα,IKKβ,TNF-α and IL-1β in the spinal cord tissues( L4 ~ L6) of inflammatory pain mice( P 〈 0. 05 or P 〈 0. 01).CONCLUSION: Resveratrol ameliorates the inflammatory pain of the mice induced by complete Freund’s adjuvant. The mechanism is related to the inhibition of NF-κB signaling pathway.
作者
王丽君
仝雷
WANG Li-jun;TONG Lei(Department of Medical Function,College of Medicine,Zhengzhou University of Industrial Technology,Department of Medical Morphology,College of Medicine,Zhengzhou University of Industrial Technolog)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2018年第2期340-345,共6页
Chinese Journal of Pathophysiology