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黄芪甲苷对神经炎症的改善作用及机制研究
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          王咪咪 ,冯永岗 ,韩 云 ,单凯欣 ,刘福宇 ,苗明三 ,方晓艳 (1. 河南中医药大学药学院,郑州
          450046;2.驻马店市中心医院药学部,河南 驻马店 463000;3.豫药全产业链研发河南省协同创新中心,郑州
          450046)
          中图分类号  R965      文献标志码  A      文章编号  1001-0408(2026)01-0030-06
          DOI  10.6039/j.issn.1001-0408.2026.01.06
          摘   要  目的  探讨黄芪甲苷对脂多糖(LPS)诱导的神经炎症的改善作用及机制。方法  将BV2细胞分为对照组、LPS组和黄芪
          甲苷20、40 μmol/L组以及地塞米松组(2 μmol/L),给药处理后,除对照组外其余各组加入1 μg/mL的LPS 以诱导神经炎症细胞模
          型,再检测各组细胞上清液中炎症因子[白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、一氧化氮(NO)]水平。将小鼠随机分为正
          常组、模型组、阳性对照组(阿司匹林肠溶片,20 mg/kg)和黄芪甲苷低、高剂量组(10、20 mg/kg),每组6只。各组小鼠灌胃/腹腔注
          射相应药物/生理盐水,每天1次,连续14 d。除正常组外,其余各组小鼠每天给药/生理盐水1 h后,腹腔注射LPS(250 μg/kg)建立
          神经炎症动物模型。末次注射LPS 2 h后,检测小鼠血清中IL-6、TNF-α水平;观察小鼠脑组织病理学形态;观察小鼠脑皮质区诱
          导型一氧化氮合酶(iNOS)/离子化钙结合衔接分子1(Iba1)和CD206/Iba1的共定位情况;检测小鼠脑组织中核因子κB(NF-κB)/丝
          裂原活化蛋白激酶(MAPK)信号通路相关蛋白[NF-κB p65、磷酸化 NF-κB p65(p-NF-κB p65)、p38 MAPK、磷酸化 p38 MAPK(p-
          p38 MAPK)、胞外信号调节激酶(ERK)、磷酸化ERK(p-ERK)]表达水平。结果  在细胞实验中,与对照组比较,LPS组细胞上清液
          中 IL-6、TNF-α、NO 水平均显著升高(P<0.05);与 LPS 组比较,各给药组细胞上清液中 IL-6、TNF-α、NO 水平均显著降低(P<
          0.05)。在动物实验中,与正常组比较,模型组小鼠血清中IL-6、TNF-α水平和脑皮质区iNOS/Iba1共定位阳性细胞数以及脑组织
          中p38 MAPK、NF-κB p65、ERK蛋白的磷酸化水平均显著升高/增多(P<0.05),脑皮质区CD206/Iba1共定位阳性细胞数显著减少
         (P<0.05),脑皮质区和海马CA3区神经元细胞排列紊乱;与模型组比较,各给药组小鼠上述定量指标均显著逆转(P<0.05),脑皮
          质区和海马CA3区神经元细胞排列较为整齐。结论  黄芪甲苷可能通过抑制NF-κB/MAPK信号通路激活,促进小胶质细胞发生
          M2型极化,进而抑制神经炎症反应。
          关键词  黄芪甲苷;小胶质细胞;炎症;表型极化;神经保护

          Improvement effects and mechanism of astragaloside Ⅳ on neuroinflammation
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          WANG Mimi ,FENG Yonggang ,HAN Yun ,SHAN Kaixin ,LIU Fuyu ,MIAO Mingsan ,FANG Xiaoyan             1, 3
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         (1.  School  of  Pharmacy,  Henan  University  of  Chinese  Medicine,  Zhengzhou  450046,  China;2.  Dept.  of
          Pharmacy,  Zhumadian  Central  Hospital,  Henan  Zhumadian  463000,  China;3.  Henan  Collaborative  Innovation
          Center  for  the  Whole  Industry  Chain  Research  and  Development  of  Traditional  Chinese  Medicine,  Zhengzhou
          450046, China)
          ABSTRACT    OBJECTIVE  To  investigate  the  improvement  effects  and  mechanism  of  astragaloside  Ⅳ  (AS- Ⅳ )  on
          lipopolysaccharide (LPS)-induced neuroinflammation. METHODS  BV2 cells were divided into control group, LPS group, AS-Ⅳ
          groups  at  concentrations  of  20  and  40  μmol/L,  and  dexamethasone  group  (2  μmol/L).  Except  for  control  group,
          neuroinflammation model was established with LPS (1 μg/mL) in other groups after medication. The levels of inflammatory factors
          [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and nitric oxide (NO)] in cell supernatant were measured in each group.
          Mice  were  randomly  divided  into  normal  group,  model  group,  positive  control  group (Aspirin  enteric-coated  tablet,  20  mg/kg),
          AS- Ⅳ  low-  and  high-dose  groups (10,  20  mg/kg),  with  6  mice  in  each  group.  Mice  in  each  group  were  administered  the
          corresponding  drug/normal  saline  via  gavage/intraperitoneal  injection,  once  a  day,  for  14  consecutive  days.  Except  for  normal
          group,  other  groups  were  intraperitoneally  injected  with  LPS (250  μg/kg)  1  hour  after  daily  administration  of  the  drug/normal
          saline  to  establish  neuroinflammation  model.  Serum  levels  of  IL-6  and  TNF- α  were  measured  2  h  after  the  last  medication;
          histopathological  morphology  of  cerebral  tissue  in  mice  were  observed;  the  co-localization  of  inducible  nitric  oxide  synthase
                                                             (iNOS)/ionized  calcium  binding  adapter  molecule  1 (Iba1)
              Δ 基金项目 国家自然科学基金项目(No.82274119);河南省重点
                                                              and  CD206/Iba1  in  the  cerebral  cortex  region  of  mice  was
          研发专项(No.251111314100);河南省科技研发计划联合基金项目
                                                              observed;  the  expressions  of  proteins  related  to  the  nuclear
         (No.222301420091)
             *第一作者 硕士研究生。研究方向:中药药理学。E-mail:                   factor-κB (NF-κB)/mitogen-activated  protein  kinase (MAPK)
          15039101896@163.com                                 signaling  pathway  in  brain  tissue  of  mice  were  also
              # 通信作者 教授,硕士生导师。研究方向:中药药理学。E-mail:              determined, including NF-κB p65, phosphorylated NF-κB p65
          fxylele@yeah.net                                   (p-NF-κB  p65),  p38  MAPK,  phosphorylated  p38  MAPK (p-


          · 30 ·    China Pharmacy  2026 Vol. 37  No. 1                                中国药房  2026年第37卷第1期
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