首页|期刊导航|中国实验动物学报|哈它各其-7联合胡麻油通过调控炎症反应与GSK3β信号通路促进压疮愈合的研究

哈它各其-7联合胡麻油通过调控炎症反应与GSK3β信号通路促进压疮愈合的研究OA

Hatagaqi-7 combined with sesame oil promotes pressure-ulcer healing via inflammation modulation and GSK3β signaling

中文摘要英文摘要

目的 本研究基于网络药理学探讨蒙药哈它各其-7 联合胡麻油对压疮创面愈合的作用机制,并采用分子对接与动物实验进行初步验证.方法 通过数据库检索及文献查阅获取哈它各其-7 联合胡麻油的潜在活性成分、作用靶点以及压疮创面对应靶点;提取共同靶点构建蛋白质相互作用网络(protein-protein interaction,PPI),并进行基因本体(gene ontology,GO)分析、京都基因与基因组百科全书分析(kyoto encyclopedia of genes and genomes,KEGG)以及分子对接.构建大鼠压疮模型,随机分为 6 组:空白(K)组、模型(M)组、哈它各其-7(Q)组、胡麻油(H)组、哈它各其-7 联合胡麻油(H+Q)组和云南白药(Y)组(每组 10只),给予相应药物干预 14 d,观察创面形态变化、创面愈合率、组织病理学变化并检测白介素-1β(interleukin-1β,IL-1β)、白介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、糖原合成酶激酶-3β(glycogen synthase kinase-3β,GSK3β)、核因子 κB p65 亚基(nuclear factor kappa-B p65 subunit,NF-κB p65)、β-连环蛋白(β-catenin)的表达水平.结果 网络药理学共筛选出 35 个活性成分、644 个药物靶点和398 个疾病靶点,核心靶点包括 BCL2、TNF-α、NFKB1、IL-6、IL-1β 和 GSK3β,主要涉及 TNF、炎症反应及 Wnt信号通路.分子对接结果显示主要活性成分咖啡因、雌二醇与 GSK3β、TNF-α、IL-1β、IL-6 核心靶点具有较好的结合能力.动物实验结果表明,哈它各其-7联合胡麻油组创面愈合率最高且胶原沉积最丰富.哈它各其-7联合胡麻油组IL-1β、IL-6、TNF-α、GSK3β 及NF-κB p65 表达下调(P<0.05),且下调幅度优于哈它各其-7组、胡麻油组及云南白药组;哈它各其-7 组、胡麻油组及云南白药组虽可下调上述指标,但与哈它各其-7 联合胡麻油组相比,呈一定上调趋势(P<0.05),哈它各其-7 联合胡麻油组 β-catenin 表达显著上调(P<0.05),且上调幅度优于哈它各其-7组、胡麻油组及云南白药组(P<0.05).结论 哈它各其-7联合胡麻油可显著促进压疮愈合,其机制可能与抑制炎症反应及调控 GSK3β 信号通路有关.表明哈它各其-7 联合胡麻油具有潜在的临床应用价值,为蒙药在压疮治疗中的转化提供实验依据.

Objective This study aimed to explore the potential mechanisms of the Mongolian medicine hatagaqi-7 combined with sesame oil in promoting pressure ulcer wound healing based on network pharmacology,and to verify the findings through molecular docking and animal experiments.Methods Potential active components and targets of hatagaqi-7 combined with sesame oil,as well as pressure ulcer-related targets,were identified through database and literature searches.The common targets were used to construct a protein-protein interaction(PPI)network,followed by gene ontology(GO)and kyoto encyclopedia of genes and genomes(KEGG)pathway analyses,and molecular docking.A rat model of pressure ulcer was established and divided into six groups:control(K),model(M),hatagaqi-7(Q),sesame oil(H),hatagaqi-7 combination sesame oil(H+Q)and yunnan baiyao(Y)groups(n=10).All groups received corresponding treatments for 14 d.Wound morphology,healing rate,histopathological changes,and the expression of interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),glycogen synthase kinase-3β(GSK3β),NF-κB p65 and β-catenin were evaluated.Results Network pharmacology identified 35 active compounds,644 drug targets,and 398 disease targets.Core targets included BCL2,TNF-α,NFKB1,IL-6,IL-1β,and GSK3β,mainly involving the TNF inflammatory response,and Wnt signaling pathways.Molecular docking indicated that the major active components-caffeine and estradiol-exhibited strong binding affinities with GSK3β,TNF-α,IL-1β,and IL-6.Animal experiments showed that the(H+Q)group had the highest wound healing rate and the most abundant collagen deposition.The expression levels of IL-1β,IL-6,TNF-α,GSK3β,and NF-κB p65 were significantly downregulated in the(H+Q)group(P<0.05),with greater reductions compared with the H,Q,Y groups(P<0.05).The expression of β-catenin was significantly upregulated in the(H+Q)group(P<0.05),and the magnitude of upregulation was significantly greater than that in the H,Q,Y groups(P<0.05).Conclusions Hatagaqi-7 combined with sesame oil significantly promotes pressure ulcer healing,potentially through suppressing inflammatory responses and regulating the GSK3β signaling pathway.The combination therapy demonstrates potential clinical value and provides an experimental basis for the application of mongolian medicine in pressure ulcer treatment.

张心雨;侯婧;杨一枭;魏林林;吴思元;宋鹤天;张志芳;刘春燕

内蒙古医科大学护理学院,呼和浩特 010000通辽市人民医院,内蒙古 通辽 028000通辽市人民医院,内蒙古 通辽 028000内蒙古医科大学护理学院,呼和浩特 010000通辽市人民医院,内蒙古 通辽 028000通辽市人民医院,内蒙古 通辽 028000内蒙古医科大学护理学院,呼和浩特 010000||通辽市人民医院,内蒙古 通辽 028000通辽市人民医院,内蒙古 通辽 028000

生物科学

哈它各其-7压疮网络药理学分子对接GSK3β

hatagaqi-7pressure ulcernetwork pharmacologymolecular dockingGSK3β

《中国实验动物学报》 2026 (7)

984-997,14

内蒙古医学科学院公立医院科研联合基金科技项目(2023GLLH0376). Funded by Science and Technology Program of the Joint Fund of Scientific Research for the Public Hospitals of Inner Mongolia Academy of Medical Sciences(2023GLLH0376).

10.3969/j.issn.1005-4847.2026.07.005

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