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减轻细菌性脑膜炎新生大鼠的神经损伤。但姜黄素与 the benefits and problems of curcumin with respect to hu‐
STAT1相互作用的精确分子模式(例如是直接结合还是 man health[J]. Molecules,2022,27(14):4400.
通过某个中间蛋白结合)仍需进一步探索。 [ 8 ] 李庆彬,岳振东,赵博,等. 姜黄素调节BDNF/TrkB信号
需要注意的是,姜黄素可同时减少细菌性脑膜炎新 通路对细菌性脑膜炎新生大鼠神经元凋亡的影响[J]. 现
生大鼠海马及皮质组织中细胞凋亡(凋亡细胞百分比显 代生物医学进展,2024,24(8):1411-1417,1438.
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著降低)和细胞焦亡(GSDMD 表达显著下调)。凋亡和
intracerebral hemorrhage-induced neuronal apoptosis and
焦亡是两种不同的程序性细胞死亡类型,但二者存在复
neuroinflammation by suppressing JAK1/STAT1 pathway
杂的交叉关系:一方面,GSDMD 作为焦亡的执行者,其
[J]. Biochem Cell Biol,2022,100(3):236-245.
不完全切割的产物可能具有促凋亡活性;另一方面,这
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两种细胞死亡方式共享STAT1/NLRP3这一上游触发信 vention of curcumin via the NLRP3 inflammasome in
[20]
号通路 。本研究结果显示,姜黄素可有效抑制STAT1/ ischemic stroke[J]. Front Pharmacol,2023,14:1249644.
NLRP3 信号通路。NLRP3 炎症小体的激活是诱导 cas‐ [11] 赵玲玲,殷萍,邹华芳,等. 新生SD大鼠细菌性脑膜炎动
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该炎症小体介导的强烈炎症环境(如高水平IL-1β)亦是 2891-2896.
促进细胞凋亡的重要刺激因素之一。因此,本课题组推 [12] LOEFFLER J M,RINGER R,HABLÜTZEL M,et al.
测,姜黄素通过靶向STAT1/NLRP3这一关键通路,从源 The free radical scavenger alpha-phenyl-tert-butyl nitrone
头上平息了“神经炎症风暴”,从而协同阻断了由此引发 aggravates hippocampal apoptosis and learning deficits in
的细胞凋亡和焦亡级联反应,这可能是该成分发挥神经 experimental pneumococcal meningitis[J]. J Infect Dis,
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保护作用的核心机制之一。
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本研究尚有一些不足之处:首先,所用改良Loeffler
hibits the activation of astrocytes and the release of inflam‐
评分法源于成年大鼠,尚缺乏适用于新生啮齿类动物的
matory cytokines in bacterial meningitis through down-
相关评分标准;其次,未能明确发生焦亡的具体细胞类
regulating HMGB1[J]. Brain Res,2021,1770:147611.
型,后续将进一步予以完善。
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综上所述,姜黄素可改善细菌性脑膜炎新生大鼠脑 ischemic stroke injury in rats by protecting the integrity of
水肿及血脑屏障损伤,减轻神经炎症,抑制细胞凋亡和 the blood-brain barrier[J]. Exp Ther Med,2021,22
焦亡,进而缓解神经损伤,其机制可能与抑制 STAT1/ (1):783.
NLRP3信号通路有关。 [15] LIU P,WANG X Y,YANG Q,et al. Collaborative action
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中国药房 2026年第37卷第1期 China Pharmacy 2026 Vol. 37 No. 1 · 23 ·

