文章摘要
张爱花,赵威东,贺慧艳,仲倩维,杨俊丽,邹 蓉.女贞子提取物对帕金森病大鼠神经炎性反应及内质网应激PERK/ATF4通路的影响[J].,2023,(15):2827-2831
女贞子提取物对帕金森病大鼠神经炎性反应及内质网应激PERK/ATF4通路的影响
Effects of Ligustrum Lucidum Extract on Neuroinflammatory Response and Endoplasmic Reticulum Stress PERK/ATF4 Pathway in Parkinson's Disease Rats
投稿时间:2023-03-07  修订日期:2023-03-31
DOI:10.13241/j.cnki.pmb.2023.15.005
中文关键词: 女贞子提取物  帕金森大鼠  神经炎性反应  内质网应激
英文关键词: Ligustrum lucidum extract  Parkinson's disease rats  Neuroinflammatory reaction  Endoplasmic reticulum stress
基金项目:山东省医药卫生科技发展计划项目(202103071006)
作者单位E-mail
张爱花 滨州医学院烟台附属医院神经内科 山东 烟台 264100 aihuavictor8@163.com 
赵威东 滨州医学院烟台附属医院康复医学科 山东 烟台 264100  
贺慧艳 滨州医学院烟台附属医院神经内科 山东 烟台 264100  
仲倩维 滨州医学院烟台附属医院神经内科 山东 烟台 264100  
杨俊丽 滨州医学院烟台附属医院神经内科 山东 烟台 264100  
邹 蓉 滨州医学院烟台附属医院神经内科 山东 烟台 264100  
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中文摘要:
      摘要 目的:探讨与分析女贞子提取物对帕金森病大鼠神经炎性反应及内质网应激蛋白激酶R样内质网激酶(PERK)/转录活化因子4(ATF4)通路的影响。方法:采用单侧注射6-羟基多巴胺(6-OHDA)毁损法建立帕金森病大鼠模型,将造模成功的大鼠36只随机平分为三组-模型组、左旋多巴组与女贞子组,每组各12只。左旋多巴组与女贞子组分别灌胃0.5 mL的左旋多巴、女贞子提取物,模型组给予无菌蒸馏水0.5 mL,2次/d,连续给药4周,检测大鼠神经炎性反应、内质网应激PERK/ATF4通路相关蛋白表达变化情况。结果:左旋多巴组与女贞子组治疗第2周、第4周的探究性反应次数显著高于模型组(P<0.05),女贞子组与左旋多巴组对比也有显著提高(P<0.05)。左旋多巴组与女贞子组治疗第2周、第4周的脑组织伊文思蓝含量显著低于模型组(P<0.05),女贞子组与左旋多巴组对比也有显著降低(P<0.05)。左旋多巴组与女贞子组治疗第2周、第4周的血清丙二醛、白介素-1β、肿瘤坏死因子-α、一氧化氮含量显著低于模型组(P<0.05),女贞子组与左旋多巴组对比也有显著降低(P<0.05)。左旋多巴组与女贞子组治疗第2周、第4周的黑质-纹状体组织PERK蛋白、ATF4蛋白相对表达水平显著低于模型组(P<0.05),女贞子组与左旋多巴组对比也有显著降低(P<0.05)。结论:女贞子提取物在帕金森病大鼠的应用能改善神经功能,降低脑组织伊文思蓝含量,还可抑制PERK/ATF4通路的激活,降低血清丙二醛、白介素-1β、肿瘤坏死因子-α、一氧化氮含量,从而持续发挥脑保护作用。
英文摘要:
      ABSTRACT Objective: To investigate and analysis the effects of Ligustrum lucidum extract on the neuroinflammatory response and the endoplasmic reticulum stress protein kinase R-like endoplasmic reticulum kinase (PERK)/transcription activating factor 4 (ATF4) pathway in Parkinson's disease rats. Methods: A rat model of Parkinson's disease was established by unilateral injection of 6-hydroxydopamine (6-OHDA). 36 cases of rats were randomly divided into three groups: model group, levodopa group and ligustrum lucidum subgroup, with 12 rats in each group. The levodopa group and ligustrum lucidum group were given 0.5 mL of levodopa and ligustrum lucidum extract by gavage respectively. The model group were given 0.5 mL of sterile distilled water twice a day for 4 weeks. The changes in the expression of protein related to the neuroinflammatory reaction and endoplasmic reticulum stress PERK/ATF4 pathway in rats were detected. Results: The number of exploratory reactions in the levodopa group and ligustrum lucidum group at the 2nd and 4th weeks of treatment were higher than that in the model group (P<0.05), and the number of exploratory reactions in the ligustrum lucidum group were also higher than that in the levodopa group (P<0.05). The content of Evans blue in brain tissue of levodopa group and ligustrum lucidum group at the 2nd and 4th weeks of treatment were lower than that of model group (P<0.05), and there were also a decrease in the ligustrum lucidum group compared with levodopa group (P<0.05). The levels of serum malondialdehyde, interleukin-1β, tumor necrosis factor- α, nitric oxide in the levodopa group and ligustrum lucidum group were lower than those in the model group at the second and fourth weeks of treatment (P<0.05), and the levels of serum malondialdehyde, interleukin-1β, tumor necrosis factor- α, nitric oxide in the ligustrum lucidum group were also lower than those in the levodopa group (P<0.05). The relative expression levels of PERK protein and ATF4 protein in substantia nigra and striatum in the levodopa group and ligustrum lucidum group were lower than those in the model group at the 2nd and 4th weeks of treatment (P<0.05), and the ligustrum lucidum group were also lower than that in the levodopa group (P<0.05). Conclusion: The application of Ligustrum lucidum extract in Parkinson's disease rats can improve the nerve function, reduce the content of Evans blue in brain tissue, inhibit the activation of PERK/ATF4 pathway, reduce the content of malondialdehyde, interleukin-1β, tumor necrosis factor- α, nitric oxide in serum, and continue to play a protective role in brain.
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