[1]刘小利,何心如,黄彦鹏.黄芩苷对坏死性小肠结肠炎新生大鼠肠损伤及NLRP3/Caspase-1/IL-1β信号通路的作用研究[J].西部中医药,2026,39(05):1-5.[doi:10.12174/j.issn.2096-9600.2026.05.01]
 LIU Xiaoli,HE Xinru,HUANG Yanpeng.Effects of Baicalin on Intestinal Injury and the NLRP3/Caspase-1/IL-1β Signaling Pathway in Neonatal Rats with Necrotizing Enterocolitis[J].Western Journal of Traditional Chinese Medicine,2026,39(05):1-5.[doi:10.12174/j.issn.2096-9600.2026.05.01]
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黄芩苷对坏死性小肠结肠炎新生大鼠肠损伤及NLRP3/Caspase-1/IL-1β信号通路的作用研究()

《西部中医药》[ISSN:2096-9600/CN:62-1204/R]

卷:
39
期数:
2026年05期
页码:
1-5
栏目:
基础研究
出版日期:
2026-05-15

文章信息/Info

Title:
Effects of Baicalin on Intestinal Injury and the NLRP3/Caspase-1/IL-1β Signaling Pathway in Neonatal Rats with Necrotizing Enterocolitis
作者:
刘小利1, 何心如2, 黄彦鹏1
1.广州中医药大学第一附属医院/广东省中医临床研究院,广东 广州 510405
2.上海中医药大学,上海 201203
Author(s):
LIU Xiaoli1, HE Xinru2, HUANG Yanpeng1
1.The First Affiliated Hospital of Guangzhou University of Chinese Medicine/Guangdong Provincial Clinical Research Academy of Traditional Chinese Medicine, Guangzhou 510405, China
2.Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
关键词:
坏死性小肠结肠炎黄芩苷NOD样受体家族3半胱氨酸天冬氨酸酶-1白细胞介素1白细胞介素18
Keywords:
necrotizing enterocolitisbaicalinNOD-like receptor family protein 3Caspase-1IL-1IL-18
分类号:
R285.5
DOI:
10.12174/j.issn.2096-9600.2026.05.01
文献标志码:
A
摘要:
目的研究黄芩苷对坏死性小肠结肠炎(necrotizing enterocolitis,NEC)新生大鼠模型肠损伤及核苷酸结合寡聚化结构域样受体蛋白3(nucleotide-binding oligomerization domain-like receptor protein 3,NLRP3)、半胱氨酸天冬氨酸酶-1(cysteinyl aspartate specific proteinase-1,Caspase-1)、白细胞介素1β(interleukin-1β,IL-1β)和IL-18的影响。 方法30只3日龄SD新生大鼠,随机分为对照组、模型组及黄芩苷组,每组10只。对照组不予任何处理,模型组及黄芩苷组新生大鼠均采用鼠奶联合配方奶粉人工喂养方式、缺氧以及冷刺激方法建立NEC模型。苏木精-伊红染色法观察肠组织病理学改变情况;蛋白免疫印迹法检测肠组织NLRP3、Caspase-1蛋白表达水平;酶联免疫吸附法检测肠组织IL-1β、IL-18表达水平。 结果与对照组比较,模型组大鼠肠组织损伤严重,病理损伤评分显著增加(P<0.05);NLRP3、Caspase-1蛋白及IL-1β和IL-18表达水平增加(P<0.05)。与模型组比较,黄芩苷组肠组织损伤评分降低,NLRP3、Caspase-1蛋白及IL-1β和IL-18表达水平降低(P<0.05)。 结论黄芩苷可能通过抑制NLRP3/Caspase-1/IL-1β信号通路,降低新生大鼠NEC发生率,而细胞焦亡可能参与新生大鼠NEC的发病过程。
Abstract:
ObjectiveTo investigate the effects of baicalin on intestinal injury and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), cysteinyl aspartate specific proteinase-1 (Caspase-1), interleukin-1β (IL-1β), and IL-18 in neonatal rat models of necrotizing enterocolitis (NEC). MethodsThirty 3-day-old neonatal SD rats were randomly divided into a control group, a model group, and a baicalin group, with 10 rats in each group. The control group received no intervention. The neonatal rats in the model group and the baicalin group were subjected to artificial feeding with a combination of rat milk and formula milk, along with hypoxia and cold stimulation, to establish the NEC model. Hematoxylin-eosin (HE) staining was used to observe histo-pathological changes in intestinal tissues; Western blot was employed to detect the protein expression levels of NLRP3 and Caspase-1 in intestinal tissues; enzyme-linked immunosorbent assay (ELISA) was performed to measure the expression levels of IL-1β and IL-18 in intestinal tissues. ResultsCompared with the control group, the model group showed severe intestinal tissue injury, with a significantly increased pathological injury score (P<0.05), and elevated expression levels of NLRP3, Caspase-1, IL-1β, and IL-18 (P<0.05). Compared with the model group, the baicalin group exhibited a decreased intestinal injury score and reduced expression levels of NLRP3, Caspase-1 protein, IL-1β, and IL-18 (P<0.05). ConclusionBaicalin may reduce the incidence of NEC in neonatal rats by inhibiting the NLRP3/Caspase-1/IL-1β signaling pathway, and pyroptosis may be involved in the pathogenesis of NEC in neonatal rats.

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备注/Memo

备注/Memo:
广东省医学科研基金(A2020616)。刘小利(1981—),女,硕士学位,主治医师。研究方向:新生儿疾病的诊治。Email:149046812@qq.com。
更新日期/Last Update: 2026-05-15