[1]赵雅,张鑫,池刚.黄芩苷通过抑制 miR-128-3p激活 Nrf2/HO-1通路减轻脓毒症大鼠肺损伤的实验研究[J].陕西中医,2026,(3):304-310.[doi:DOI:10.3969/j.issn.1000-7369.2026.03.003]
　ZHAO Ya,ZHANG Xin,CHI Gang.Experimental study of baicalin alleviating lung injury in septic rats by inhibiting miR-128-3p and activating the Nrf2/HO-1 pathway[J].,2026,(3):304-310.[doi:DOI:10.3969/j.issn.1000-7369.2026.03.003]
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黄芩苷通过抑制 miR-128-3p激活 Nrf2/HO-1通路减轻脓毒症大鼠肺损伤的实验研究

《陕西中医》[ISSN:1000-7369/CN:61-1281/TN]

卷:
期数:
2026年3期
页码:
304-310
栏目:
基础研究
出版日期:
2026-03-05

文章信息/Info

Title:
Experimental study of baicalin alleviating lung injury in septic rats by inhibiting miR-128-3p and activating the Nrf2/HO-1 pathway
作者:
赵雅1; 张鑫2; 池刚3
（1.长治市人民医院，山西 长治 046000;2.长治医学院附属和济医院，山西 长治 046000;3.长治医学院基础医学部生物化学与分子生物学教研室，山西 长治 046000)
Author(s):
ZHAO Ya1; ZHANG Xin2; CHI Gang3
(1.Changzhi People’s Hospital,Changzhi 046000,China;2.Heji Hospital Affiliated to Changzhi Medical College,Changzhi 046000,China;3.Department of Biochemistry and Molecular Biology,Department of Basic Medicine,Changzhi Medical College,Changzhi 046000,China)
关键词:
脓毒症; 肺损伤; 黄芩苷; miR-128-3p; Nrf2/HO-1通路; 氧化应激
Keywords:
Sepsis; Lung injury; Baicalein; miR-128-3p; Nrf2/HO-1 pathway; Oxidative stress
分类号:
R 631
DOI:
DOI:10.3969/j.issn.1000-7369.2026.03.003
文献标志码:
A
摘要:
目的：本研究旨在探讨黄芩苷通过抑制 miR-128-3p 对脓毒症诱导的大鼠肺损伤的影响及机制。方法：采用盲肠结扎穿孔术（CLP）建立脓毒症模型，将 SD 大鼠随机分为 CLP 组、Sham 组、低剂量组、高剂量组、NC 组和 miR-128-3p 组，分别给予不同处理，观察肺组织病理变化、肺水肿程度及炎症因子等指标。同时对大鼠肺泡巨噬细胞 NR8383 进行转染和药物干预实验。结果：CLP 术后大鼠肺组织中 miR-128-3p 表达升高，黄芩苷可减轻肺损伤和肺水肿，降低炎症因子水平，且高剂量效果更显著；在细胞实验中，LPS 刺激可降低 NR8383 细胞活力，黄芩苷则能增强细胞活力并降低炎症因子释放。进一步研究发现，miR-128-3p 过表达会加重肺损伤及炎症反应，而黄芩苷能降低 miR-128-3p 表达并逆转其引发的细胞活力下降和炎症因子释放增加。结论：黄芩苷通过抑制 miR-128-3p 可减轻脓毒症诱导的大鼠肺损伤，其机制可能与调节细胞凋亡、炎症反应及氧化应激有关，为脓毒症肺损伤治疗提供了新靶点和实验依据。
Abstract:
Objective:This study aimed to explore the impact and mechanism of baicalein on sepsis-induced rat lung injury through inhibiting miR-128-3p.Methods:A sepsis model was established using cecal ligation and puncture (CLP).SD rats were randomly divided into CLP,Sham,low-dose,high-dose,NC,and miR-128-3p groups,each receiving different treatments.Pathological changes in lung tissue,degree of lung edema,and inflammatory factors were observed.Additionally,transfection and drug intervention experiments were conducted on rat alveolar macrophages NR8383.Results:Post-CLP,miR-128-3p expression in rat lung tissue increased.Baicalein alleviated lung injury and edema and reduced inflammatory factors,with more significant effects at high doses.In cell experiments,LPS reduced NR8383 cell viability,while baicalein enhanced viability and decreased inflammatory factor release.Further research indicated that overexpressing miR-128-3p worsened lung injury and inflammation,whereas baicalein downregulated miR-128-3p expression and reversed the cell viability decrease and increased inflammatory factor release caused by miR-128-3p.Conclusion:Baicalein,by inhibiting miR-128-3p,mitigates sepsis-induced rat lung injury.This mechanism may involve regulating apoptosis,inflammation,and oxidative stress,providing a new target and experimental basis for treating sepsis-induced lung injury.

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备注/Memo

备注/Memo:
山西省基础研究计划项目（202403021222718）
更新日期/Last Update: 2026-03-05