柚皮苷对脑梗死大鼠的保护作用及其机制研究  

Protective Effect of Naringin on Cerebral Infarction in Rats and Its Mechanism

作　　者：段婷婷 王进华[1] 邵菲菲 DUAN Tingting;WANG Jinhua;SHAO Feifei

机构地区：[1]衢州市人民医院神经内科,浙江衢州324000

出　　处：《新中医》2022年第3期1-7,共7页New Chinese Medicine

摘　　要：目的:探讨柚皮苷对Wistar大鼠脑梗死过程中炎症通路以及炎性坏死的影响,及认识柚皮苷改善脑梗死的分子机制。方法:将Wistar大鼠随机分为假手术组、单纯模型组及柚皮苷组,造模成功后检测柚皮苷干预后Wistar大鼠的神经功能改变以及脑组织的梗死面积。检测柚皮苷干预后Wistar大鼠血清中乳酸脱氢酶以及炎症相关因子肿瘤坏死因子-α及白细胞介素-1β的水平。此外,体外水平检测柚皮苷对缺氧损伤对人脑胶质细胞(HEB细胞)活性的影响,通过检测炎症坏死相关因子的表达以及高迁移率族蛋白B1 (HMGB1)/Toll样受体4 (TLR4)/核转录因子-κB (NF-κB)通路的激活水平探究柚皮苷改善炎症和坏死的分子机制。结果:给予Wistar脑梗死大鼠柚皮苷后其神经能损伤明显改善,神经功能损伤评分低于单纯模型组,差异有统计学意义(P<0.05),同时脑梗死面积也较单纯模型组显著降低。血清肿瘤坏死因子-α及白细胞介素-1β水平以及乳酸脱氢酶水平在柚皮苷处理后的脑梗死大鼠中明显降低。在细胞水平,柚皮苷对缺氧环境中的细胞保护作用较为明显,细胞活性明显高于低氧组。在分子水平,Western blotting结果显示柚皮苷可以通过抑制HMGB1/TLR4/NF-κB通路下调脑梗死中炎症通路的激活。结论:柚皮苷可通过抑制HMGB1/TLR4/NF-κB通路下调炎症和细胞坏死相关因子的表达,对脑梗死损伤具有一定的保护作用。Objective:To investigate the effects of naringin on inflammatory pathway and inflammatory necrosis during cerebral infarction in Wistar rats, and to understand the molecular mechanism of naringin in improving cerebral infarction.Methods: Wistar rats were randomly divided into sham operation group, simple model group and naringin group.After naringin intervention, the changes of neurological function and infarct area of brain tissue were detected. After naringin intervention, lactate dehydrogenase and inflammatory related factor tumor necrosis factor-α in serum and level of interleukin-1β of Wistar rats were detected.In addition,the effect of naringin on the activity of human brain glial cells(HEB cells) after hypoxia injury was detected in vitro,and the expression of inflammatory necrosis related factors and high mobility group box1(HMGB1)/Toll-link receptosrs 4(TLR4)/nuclear factor-κB(NF-κB) were detected. Results:After administration of naringin to Wistar rats with cerebral infarction, the nerve energy injury was significantly improved, the score of nerve function injury was significantly lower than that of the simple model group(P<0.05),and the cerebral surface infarct area was significantly lower than that of the simple model group.Serum tumor necrosis factor-α and interleukin-1β and the levels of and lactate dehydrogenase in cerebral infarction rats treated with naringin decreased significantly. At the cellular level,naringin has an obvious protective effect on cells in hypoxic environment,and the cell activity is significantly higher than that in hypoxia group. At the molecular level, Western blotting results show that naringin can inhibit HMGB1/TLR4/NF-κB.Conclusion:Naringin can inhibit HMGB1/TLR4/NF-κB pathway down regulates the expression of inflammatory and necrosis related factors,which has a certain protective effect on cerebral infarction injury.

关 键 词：脑梗死 柚皮苷 炎症 细胞坏死 

分 类 号：R285.5[医药卫生—中药学]