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症因子的产生,尤其是抑制促炎因子的分泌,可以减轻                                 al.  Protective  effects  of  propolis  and  chitosan  nanopar‐
          炎症反应。本研究结果显示,LPS 刺激 RAW264.7 细胞                          ticles  against  ibuprofen-induced  hepatotoxicity  in  albino
          能显著升高NO、TNF-α、IL-6、IL-1β含量,表明体外炎症                        rats[J]. Diseases,2024,12(3):49.
          模型建立成功;经 OA 处理后能够显著促进 IL-4、IL-10                    [ 5 ]  广西壮族自治区卫生厅 . 广西中药材标准:第二册[M].
          释放,降低NO、TNF-α、IL-6、IL-1β含量并能抑制TNF-α、                     南京:广西科学出版社,1996:20-21.
                                                                   Department  of  Health  of  Guangxi  Zhuang  Autonomous
          IL-6、IL-1β mRNA表达。这些结果表明OA能抑制LPS
                                                                   Region.  Guangxi  traditional  Chinese  medicine  standards:
          诱导RAW264.7细胞的炎症反应,具有良好的抗炎活性。
                                                                   volume 2[M]. Nanning:Guangxi Science Press,1996:20-21.
              NF-κB通路是LPS诱导炎症因子表达的关键通路,
                                                              [ 6 ]  WU  Z  N,DAI  X Y,WANG W  Z,et  al.  Polyprenylated
          在细胞中主要以 p50/p65 异源二聚体形式存在;在 LPS                          benzophenones and tocotrienol derivatives from the edible
          刺激下,p50/p65 二聚体易位到细胞核引起下游多种基                             fruits of Garcinia oblongifolia champ. ex Benth. and their
                  [11]
          因的表达 。p65 是调控炎症反应的关键蛋白,因此抑                               cytotoxicity  activity[J].  J  Agric  Food  Chem,2022,70
          制 NF-κB p65 是治疗炎症性疾病的关键靶点和有效治                           (34):10506-10520.
          疗策略。本研究结果显示,OA 能够显著抑制 LPS 诱导                        [ 7 ]  SUKANDAR E R,KAENNAKAM S,WONGSUWAN S,
          的 RAW264.7 细胞中 NF-κB p65、IκBα 蛋白磷酸化表达                    et  al.  Schomburginones  A-J,geranylated  benzophenones
          和 IκBα 蛋白降解,且抑制 NF-κB p65 核易位,表明 OA                      from  the  leaves  of  Garcinia  schomburgkiana  and  their
          可能通过抑制 NF-κB 通路对 LPS 诱导的 RAW264.7 细                      cytotoxic  and  anti-inflammatory  activities[J].  Phytochemi-
          胞发挥抗炎作用。                                                 stry,2023,211:113701.
              已有研究表明,内源性自由基如ROS在宿主防御中                         [ 8 ]  YANG X X,LIU Z G,FANG M Y,et al. Novel pterostil‐
                                                                   bene derivatives ameliorate heart failure by reducing oxi‐
          起关键作用,但过量的 ROS 可引发和促进炎症性疾
                                                                   dative  stress  and  inflammation  through  regulating  Nrf2/
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          病 。ROS 还可和 NO 协同作用,增强氧化应激和损                              NF-κB signaling pathway[J]. Eur J Med Chem,2023,
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          伤 。 本 研 究 结 果 表 明 ,OA 显 著 抑 制 LPS 诱 导 的
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          RAW264.7 细胞中 ROS 的积累。Nrf2 是细胞介导抗氧                   [ 9 ]  LIU  W,YU  M  Y,XIE  D,et  al.  Melatonin-stimulated
          化应激反应的关键转录因子,生理条件下Nrf2与Keap1                             MSC-derived  exosomes  improve  diabetic  wound  healing
          在细胞质中联合;应激状态下 Nrf2 被活化,Nrf2 就会从                          through  regulating  macrophage  M1  and  M2  polarization
          Keap1 中解离并转移到细胞核中,激活其下游 HO-1、                            by  targeting  the  PTEN/Akt  pathway[J].  Stem  Cell  Res
          NQO1等多种抗氧化因子的表达,启动抗氧化,快速清除                               Ther,2020,11(1):259.
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          ROS,从而减轻氧化损伤 。HO-1 是一种细胞保护酶,                        [10]  YANG F M,FAN D,YANG X Q,et al. The artemisinin
          具有限速酶的作用,其受 Nrf2 调控,并催化血红素降解                             analog SM934 alleviates dry eye disease in rodent models
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          为胆绿素、碳氧化物和铁 。本研究结果显示,OA能够                                by regulating TLR4/NF-κB/NLRP3 signaling[J]. Acta
          显著抑制 Keap1 蛋白表达,增加 Nrf2、HO-1 和 NQO1 蛋                    Pharmacol Sin,2021,42(4):593-603.
          白表达水平,并促进 Nrf2 向细胞核易位,表明 OA 能够                      [11]  YU  H,LIN  L  B,ZHANG  Z  Q,et  al. Targeting  NF- κB
                                                                   pathway for the therapy of diseases:mechanism and clini‐
          通过激活Nrf2通路发挥抗炎、抗氧化的作用。
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              综上所述,OA能够抑制LPS诱导的RAW264.7细胞
          炎症,其作用机制可能与抑制 NF-κB 通路、激活 Nrf2 通                        (1):209.
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          路、减少ROS和炎症因子的过度释放有关。
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          参考文献                                                     reactive  oxygen  species  scavenging  in  wound  healing[J].
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          · 1214 ·    China Pharmacy  2024 Vol. 35  No. 10                            中国药房  2024年第35卷第10期
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