宽缨酮靶向抑制STAT3减轻线粒体功能障碍和炎症缓解急性肾损伤

doi:10.12122/j.issn.1673-4254.2026.03.11

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (3): 570-581.doi: 10.12122/j.issn.1673-4254.2026.03.11

• 基础研究 • 上一篇

宽缨酮靶向抑制STAT3减轻线粒体功能障碍和炎症缓解急性肾损伤

刘泽¹(), 毛樟坤², 尤达³, 王俊杰⁴, 何咏梅¹, 余伊雯², 文志强², 方会龙²(), 何汶霞¹()

^1.湘南学院，护理学院，湖南郴州 423000
^2.湘南学院，基础医学院，湖南郴州 423000
^4.湘南学院，药学院，湖南郴州 423000
^3.湖南省人民医院全科医学科，湖南长沙 410000

收稿日期:2025-08-16 出版日期:2026-03-20 发布日期:2026-03-26
通讯作者: 方会龙,何汶霞 E-mail:liuze0113@xnu.edu.cn;fanghuilong@xnu.edu.cn;602743915@qq.com
作者简介:刘泽，博士，副教授，E-mail: liuze0113@xnu.edu.cn
基金资助:
湖南省自然科学基金青年项目(2023JJ40609);湖南省教育厅科学研究重点项目(23A0596);湖南省科技厅创新型省份专项郴州产业要素科技创新服务建设平台项目(22sfq51);生物医药产业化中试技术研发公共服务平台(4692201);湘南学院-郴州产业技术研究院科技与成果转化平台建设(2023sfq10)

Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation

Ze LIU¹(), Zhangkun MAO², Da YOU³, Junjie WANG⁴, Yongmei HE¹, Yiwen YU², Zhiqiang WEN², Huilong FANG²(), Wenxia HE¹()

^1.School of Nursing, Xiangnan University, Chenzhou 423000, China
^2.School of Basic Medical Sciences, Xiangnan University, Chenzhou 423000, China
^4.School of Pharmacology, Xiangnan University, Chenzhou 423000, China
^3.Department of General Practice, Hunan Provincial People's Hospital, Changsha 410000, China

Received:2025-08-16 Online:2026-03-20 Published:2026-03-26
Contact: Huilong FANG, Wenxia HE E-mail:liuze0113@xnu.edu.cn;fanghuilong@xnu.edu.cn;602743915@qq.com

摘要/Abstract

摘要：

目的探究宽缨酮（EN）减轻缺血再灌注（IR）诱导的小鼠急性肾损伤（AKI）的作用机制。方法 24只雄性C57BL/6J小鼠随机分为Sham、IR及EN低、高剂量组4组（6只/组）。双侧肾蒂IR处理构建AKI模型，EN低、高剂量组在术前2 d腹腔注射EN（0.25、1.0 mg·kg^-1·d^-1）直至组织取材前1 d。采用网络药理学分析EN作用通路和分子机制，采用分子对接分析EN与靶点的结合性能。检测小鼠肾功能、肾组织病理、肾小管损伤指标（KIM-1、NGAL）、p-STAT3、p-PI3K及p-JAK2的表达、EN与STAT3相互作用、炎症及线粒体生物发生及其功能。另将24只雄性C57BL/6J小鼠随机分为：Sham、IR、IR+EN和IR+EN+ML115（STAT3激动剂）组4组（6只/组），分析STAT3在EN减轻IR诱导的AKI中的作用机制。结果低、高剂量EN均减轻小鼠肾组织损伤、改善肾功能，包括降低血肌酐、尿素氮、肾小管损伤评分及下调KIM-1和NGAL的表达（P<0.05）。网络药理学分析发现EN核心靶点富集信号通路与炎症密切相关。低、高剂量EN均降低AKI小鼠肾组织炎症因子（IL-6、MCP-1、TNF-α）的水平及肾间质巨噬细胞浸润（P<0.05），增加肾组织ATP含量及线粒体DNA拷贝数（P<0.05），并上调PGC-1α、TFAM、Nrf2的基因表达以及PGC-1α、TOM20的蛋白表达（P<0.05）。基于分子对接结果筛选出STAT3和PI3K为EN减轻AKI的关键靶点。动物实验结果显示，EN抑制AKI小鼠肾组织p-STAT3和p-PI3K表达（P<0.05），但不影响p-JAK2的表达（P>0.05）。表面等离子共振实验证实EN特异性结合STAT3。ML115可逆转EN对AKI小鼠的肾功能、肾组织病理损伤、肾小管损伤及炎症反应的保护作用（P<0.05）。结论 EN通过靶向抑制STAT3促进线粒体生物发生，减轻肾脏线粒体功能损伤及炎症反应，从而缓解IR诱导的AKI。

关键词: 宽缨酮, 急性肾损伤, 缺血再灌注, STAT3, 线粒体生物发生, 炎症反应

Abstract:

Objective To investigate the mechanism of eurycomanone (EN) for ameliorating ischemia/reperfusion (IR)-induced acute kidney injury (AKI) in mice. Methods Twenty-four male C57BL/6J mice were randomly divided into 4 groups (n=6) for sham operation, IR modeling by bilateral renal pedicle clamping, or intraperitoneal injections of EN at 0.25 or 1.0 mg/kg for two days prior to surgery. Network pharmacology and molecular docking were used to identify the potential molecular targets and signaling pathways and evaluate the binding affinities. Renal function, histopathological changes, expression of tubular injury markers (KIM-1 and NGAL), phosphorylation levels of STAT3, PI3K, and JAK2, renal inflammation, mitochondrial biogenesis, and mitochondrial function of the mice were assessed. The interaction between EN and STAT3 was examined using surface plasmon resonance (SPR). Another 24 male C57BL/6J mice receiving sham operation, IR modeling, or EN or EN+ML115 (a STAT3 agonist) treatment prior to modeling (n=6) were used to validate the role of STAT3 in EN-mediated renal protection. Results Both low- and high-dose EN significantly alleviated renal injury and improved renal function in mice with IR-induced AKI. The core targets of EN were associated with inflammation-related signaling pathways. EN treatment markedly reduced renal levels of IL-6, MCP-1, and TNF-αand decreased macrophage infiltration (F4/80-positive cells) in renal interstitial tissue of the mice. EN also significantly increased renal ATP content and mitochondrial DNA copy number (P<0.05), and upregulated the expressions of PGC-1α, TFAM, and Nrf2 mRNAs and protein levels of PGC-1α and TOM20. Molecular docking identified STAT3 and PI3K as key molecular targets of EN. In mice with IR-induced AKI, EN significantly suppressed phosphorylation of STAT3 and PI3K in the renal tissues without affecting p-JAK2 levels. SPR analysis confirmed a direct and specific interaction between EN and STAT3. Notably, activation of STAT3 by ML115 significantly reversed the renoprotective effects of EN. Conclusion EN mitigates IR-induced AKI in mice by directly binding to STAT3 to inhibit its phosphorylation, suppressing inflammation, and enhancing mitochondrial biogenesis and function, suggesting the potential of EN as a promising therapeutic candidate for IR-induced AKI.

Key words: eurycomanone, acute kidney injury, ischemia-reperfusion, STAT3, mitochondrial biogenesis, inflammation

刘泽, 毛樟坤, 尤达, 王俊杰, 何咏梅, 余伊雯, 文志强, 方会龙, 何汶霞. 宽缨酮靶向抑制STAT3减轻线粒体功能障碍和炎症缓解急性肾损伤[J]. 南方医科大学学报, 2026, 46(3): 570-581.

Ze LIU, Zhangkun MAO, Da YOU, Junjie WANG, Yongmei HE, Yiwen YU, Zhiqiang WEN, Huilong FANG, Wenxia HE. Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation[J]. Journal of Southern Medical University, 2026, 46(3): 570-581.

图/表 10

表1 基因引物序列

Tab.1 Primer sequence for qRT-PCR

Gene name	Forward (5′-3′)	Reverse (5′-3′)
NGAL	ATGTCACCTCCATCCTGGTCAG	GCCACTTGCACATTGTAGCTCTG
KIM-1	ACATATCGTGGAATCACAACGAC	ACTGCTCTTCTGATAGGTGACA
TNF-α	CAGGCGGTGCCTATGTCTC	CGATCACCCCGAAGTTCAGTAG
MCP-1	TAAAAACCTGGATCGGAACCAAA	GCATTAGCTTCAGATTTACGGGT
IL-6	CTGCAAGAGACTTCCATCCAG	AGTGGTATAGACAGGTCTGTTGG
PGC-1α	TGAACGCACCTTAAGTGTGGAA	GGGTTATCTTGGTTGGCTTTATGA
TFAM	CACCCAGATGCAAAACTTTCAG	CTGCTCTTTATACTTGCTCACAG
Nrf2	AAAGCACAGCCAGCACATTC	GGGATTCACGCATAGGAGCA
GAPDH	GGTGAAGGTCGGTGTGAACG	CTCGCTCCTGGAAGATGGTG
ND1	GGATCCGAGCATCTTATCCA	GGTGGTACTCCCGCTGTAAA
S18	TTCCAGCACATTTTGCGAGTA	CACGCCCTTAATGGCAGTGAT

图1 EN减轻IR诱导的小鼠AKI

Fig.1 EN pretreatment alleviates ischemia/reperfusion (IR)-induced acute kidney injury (AKI) in mice. A: Schematic diagram of the animal study protocol. B, C: SCr and BUN levels in each group. D: HE staining showing the renal injury in the mice. The lower panels (Scale bar=50 μm) are magnified images of the boxed areas in the upper panels (Scale bar=100 μm). Asterisks indicate damaged tubules. E: Quantitative assessment of renal injury. F, G: qRT-PCR for detecting mRNA levels of KIM-1 and NGAL in the renal tissues. H-J: Western blotting for KIM-1 and NGAL expressions. #P<0.05 vs sham group, *P<0.05 vs IR group, ※P<0.05 vs IR+EN-L group (n=6).

图2 交集靶点的GO和KEGG富集分析

Fig.2 GO and KEGG enrichment analysis of the intersection targets. A: Molecular structure of EN. B: Venn diagram of the EN targets, IR targets and AKI targets. C-E: Top 10 items for the biological process (BP), molecular functional (MF) and cellular component (CC) enrichment analysis in GO enrichment analysis. F: The top 8 inflammatory enrichment signaling pathways from KEGG pathway enrichment analysis.

图3 EN抑制IR-AKI小鼠肾脏炎症

Fig.3 EN suppresses renal inflammation in mice with IR-induced AKI in mice. A-C: qRT-PCR for detecting mRNA levels of MCP-1, TNF‑α and IL-6. D, E: Immunofluorescence staining showed infiltration of F4/80-positvie cells (arrows) in mouse renal tissues (Scale bar=50 μm). #P<0.05 vs sham group, *P<0.05 vs IR group, ※P<0.05 vs IR+EN-L group (n=6).

图4 EN通过促进线粒体生物发生改善IR-AKI小鼠肾脏线粒体功能

Fig.4 EN rescues renal mitochondrial function by promoting mitochondrial biogenesis in mice with IR-induced AKI. A: Quantification of ATP content. B: Quantification of mtDNA copy number. C-E: qRT-PCR for detecting mRNA level of PGC-1α, TFAM and Nrf2. F-H: Western blotting for PGC-1α and TOM 20 expressions. #P<0.05 vs sham group, *P<0.05 vs IR group, ※P<0.05 vs IR+EN-L group (n=6).

图5 PPI网络与C-T网络的构建

Fig.5 Construction of the protein-protein interaction (PPI) network and compound-target (C-T) network. A: The PPI network among the potential targets of EN against IR-induced AKI. B: The C-T network between EN and the potential targets. Square: EN compound; Circle: Predicted targets.

表2 EN与核心靶点分子对接结果

Tab.2 Molecular docking of EN with the core targets

Target	Score	Degree	RCSB ID
STAT3	-7.7	24	6QHD
PIK3CA	-9.1	15	8BFU
TLR4	-6.7	15	2Z62
PIK3R1	-6.8	14	1PHT
PIK3CB	-9.0	13	2Y2A
PIK3CD	-8.2	13	5IS5
HSP90AB1	-7.4	12	2NMQ
PTPN11	-8.7	11	3O5X
HIF1A	-7.9	10	1H2K
HDAC2	-9.2	10	4LXZ
PDGFRB	-6.7	10	1H9O
ITGB1	-8.1	9	4DX9
NR3C1	-7.4	9	3BQD
PIK3CG	-8.6	9	2CHW
PDGFRA	-7.5	8	5GRN
RXRA	-7.3	8	4N5G
PRKCD	-7.0	8	1YRK
NFKB1	-7.2	8	7LEQ
AR	-6.6	8	1E3G

图6 EN与核心靶点的分子对接可视化

Fig.6 Visualization of molecular docking between the core targets and EN. A: Schematic diagram of molecular docking between EN and STAT3. B-F: Schematic diagram of molecular docking between EN with different subunits of PI3K, including PIK3CA, PIK3CB, PIK3CD, PIK3CG and PIK3R1.

图7 EN直接靶向STAT3并抑制其磷酸化

Fig.7 EN suppresses phosphorylation of STAT3 by binding to STAT3. A-C: Western blotting for p-STAT3, STAT3, p-PI3K and PI3K expressions in the renal tissues. D-E: Western blotting for p-JAK2 and JAK2 expressions in the renal tissues. #P<0.05 vs sham group, *P<0.05 vs IR group, ※P<0.05 vs IR+EN-L group (n=6). F: SPR test using Biacore demonstrating the stable fit of the interaction between EN and STAT3.

图8 STAT3激动剂ML115能够逆转EN对IR-AKI小鼠的肾损伤及炎症反应

Fig.8 STAT3 agonist ML115 reduces EN-mediated renal and anti-inflammatory protection in IR-AKI mice. A, B: SCr and BUN levels in each group. C: Quantitative assessment of renal injury. D: HE staining show the morphological injury. The lower panels (Scale bar=50 μm) are magnified images of the boxed areas in the upper panels (Scale bar=100 μm). Asterisks indicate damaged tubules. E, F: qRT-PCR for detecting mRNA levels of KIM-1 and NGAL in the renal tissues. G-I: Western blotting for KIM-1 and NGAL expressions. J-L: qRT-PCR for detecting mRNA levels of MCP-1, TNF-α and IL-6. #P<0.05 vs sham group, *P<0.05 vs IR group, ※P<0.05 vs IR+EN group (n=6).

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宽缨酮靶向抑制STAT3减轻线粒体功能障碍和炎症缓解急性肾损伤

Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation

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