摘要
目的:探究化橘红(ECG)对脑缺血再灌注损伤(CIRI)大鼠模型脑组织及认知功能的影响。方法:将SD大鼠随机分为假手术组、模型组、ECG低剂量组、ECG中剂量组、ECG高剂量组和尼莫地平组,每组10只。除假手术组外其余各组通过线栓法构建大鼠大脑中动脉闭塞模型。干/湿法检测脑含水量;Longa法评价大鼠神经功能损伤;苏木素-伊红(HE)染色检查脑组织病理变化;跳台试验测试犯错次数;Y迷宫实验记录新异臂进入次数;酶联免疫吸附法(ELISA)检测白细胞介素(IL)-6、诱导型一氧化氮合酶(i NOS)和肿瘤坏死因子(TNF)-α水平;试剂盒检测超氧化物歧化酶(SOD)、丙二醛(MDA)含量;蛋白免疫印迹法(Western Blot)检测脑源性神经营养因子(BDNF)、神经生长因子(NGF)、Toll样受体4(TLR4)、髓样分化因子88(MyD88)、核转录因子-κB(NF-κB)p65、磷酸化核转录因子-κB(p-NF-κB)p65蛋白表达水平。结果:与假手术组比较,模型组大鼠脑含水量、神经功能缺损评分、犯错次数、MDA含量和IL-6、i NOS和TNF-α水平升高,TLR4、MyD88蛋白表达水平和NF-κB p65/p-NF-κB p65比值升高,新异臂进入次数、BDNF、NGF蛋白表达水平和SOD含量降低(P<0.05);与模型组相比较,ECG中剂量组、ECG高剂量组和尼莫地平组大鼠脑含水量、神经功能缺损评分、犯错次数、MDA含量和IL-6、i NOS和TNF-α水平降低,TLR4、MyD88蛋白表达水平和NF-κB p65/p-NF-κB p65比值降低,新异臂进入次数、BDNF、NGF蛋白表达水平和SOD含量升高(P<0.05)。结论:ECG可能介导NF-κB信号通路改善CIRI大鼠模型脑组织损伤及认知功能。
Objective:To explore the effects of exocarpium citri grandis(ECG)on brain tissue injury and cognitive function in mice with cerebral ischemia-reperfusion injury(CIRI).Methods:SD mice were randomly divided into sham group,model group,ECG low-dose group,ECG mid-dose group,ECG high-dose group,and nimodipine group,with 10 mice in each group.The model of middle cerebral artery occlusion was established in all groups except sham group.The moisture content of brain was measured by dry/wet method.Longa method was used to evaluate nerve function injury in mice.Hematoxylin-eosin(HE)staining was used to detect the pathological injury of brain tissue.Platform test detected the number of mistakes.Y Maze test recorded the entry times of new arms.The levels of interleukin-6(IL-6),inducible nitric oxide synthase(iNOS),and tumor necrosis factor(TNF)-αwere detected by enzyme-linked immunosorbent assay(ELISA).The protein expression levels of brain-derived neurotrophic factor(BDNF),nerve growth factor(NGF),Toll-like receptor 4(TLR4),myeloid differentiation factor 88(MyD88),nuclear transcription factor-κB(NF-κB)p65,and phosphorylated nuclear transcription factor-κB(p-NF-κB)p65 were examined using Western Blot.Results:Compared with sham group,brain water content,neurological deficit score,times of mistakes,MDA content,IL-6,iNOS,and TNF-αlevels increased in model group,TLR4,MyD88 protein expression levels and NF-κB p65/p-NF-κB p65 ratio increased,number of new arm entry,the expression levels of BDNF and NGF protein and SOD content decreased(P<0.05).Compared with model group,brain water content,neurological deficit score,times of mistakes,MDA content and IL-6,iNOS,and TNF-αlevels of mice in the medium dose group,high dose group,and nimodipine group decreased,the expression levels of TLR4 and MyD88 protein and the ratio of NF-κB p65/P-NF-κB p65 decreased,while number of new arm entry,the expression levels of BDNF and NGF protein,and SOD content increased(P<0.05).Conclusion:ECG may mediate NF-κB signaling pathway to protect brain tissue and improve cognitive function in mice with CIRI.
作者
刘雪霜
罗君
王凯
李卫
王璞
LIU Xueshuang;LUO Jun;WANG Kai;LI Wei;WANG Pu(Dazhou Vocational College of Traditional Chinese Medicine,Dazhou 635000,Sichuan,China;Dazhou Integrated Traditional Chinese and Western Medicine Hospital(Affiliated Hospital of Dazhou Vocational College of Traditional Chinese Medicine))
出处
《中西医结合心脑血管病杂志》
2025年第9期1331-1337,共7页
Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基金
达州市社会科学研究“十四五”规划项目(No.DZ22D116)。
关键词
脑缺血再灌注损伤
化橘红
炎性因子
核转录因子-κB信号通路
cerebral ischemia-reperfusion injury
exocarpium citri grandis
inflammatory factor
nuclear transcription factor-κB signaling pathway
