Xin Sheng Hua Granule ameliorate chemotherapy-induced blood deficiency syndrome through ihibiting JAK1/STAT1 pathway activation

IF 2.5 3区 医学 Q3 CHEMISTRY, MEDICINAL
Jie Luo , Pei-Feng Zhu , Xiao-Li Li, Jun-Ying Huang, Qiong Jin, Xi Zhang, Lu Liu
{"title":"Xin Sheng Hua Granule ameliorate chemotherapy-induced blood deficiency syndrome through ihibiting JAK1/STAT1 pathway activation","authors":"Jie Luo ,&nbsp;Pei-Feng Zhu ,&nbsp;Xiao-Li Li,&nbsp;Jun-Ying Huang,&nbsp;Qiong Jin,&nbsp;Xi Zhang,&nbsp;Lu Liu","doi":"10.1016/j.fitote.2025.106571","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>As a classic prescription for postpartum diseases in traditional Chinese medicine prescriptions, Xin Sheng Hua Granule (XSHG) exerts pharmacological activities such as promoting blood circulation and removing blood stasis. However, its mechanism remains incompletely elucidated to date.</div></div><div><h3>Purpose</h3><div>To analyze the nascent particles by Ultra Performance Liquid Chromatography-Quadrupole-Time-of-Flight/Mass Spectrometry (UPLC-Q-TOF/MS), to explore the effectiveness of XSHG on blood deficiency syndrome, and to clarify its material basis and potential mechanism.</div></div><div><h3>Methods</h3><div>The chemical composition of nascent particles was qualitatively analyzed by UPLC-Q-TOF/MS. The mechanism of XSHG in alleviating blood deficiency syndrome was predicted using network pharmacology, and its effects were further investigated by establishing a rat model of blood deficiency. The expression of related proteins in the Janus Kinase 1 (JAK1)/ Signal Transducer and Activator of Transcription 1 (STAT1) signaling pathway and inflammatory proteins were examined using the methods such as Hematoxylin and Eosin (H&amp;E), Real-Time Reverse Transcription PCR (qRT-PCR), Immunohistochemistry (IHC) and Western Blotting (WB) to elucidate the underlying protective mechanisms of XSHG in mitigating Blood Deficiency Syndrome (BDS).</div></div><div><h3>Results</h3><div>A total of 109 compounds were identified from the nascent particles. Network pharmacology research reveals that the mechanism of XSHG in the treatment of BDS may be related to the JAK1/STAT1 signaling pathway. In experiments, XSHG significantly protected mice against Cyclophosphamide (CTX) and APH-induced BDS by attenuating spleen histological changes and activities of Erythropoietin (EPO), (Granulocyte-Macrophage Colony-Stimulating Factor) GM-CSF. The BDS with CTX and APH-induced was inhibited by XSHG as confirmed by the inhibition of Tumor Necrosis Factor-alpha (TNF-<em>α</em>), Interleukin-1 beta (IL-1<em>β</em>) and Interleukin-6 (IL-6) production. Furthermore, CTX and APH-induced expression of JAK1 and STAT1, and activation of nuclear factor-<em>κ</em>B (NF-<em>κ</em>B) were significantly suppressed by XSHG.</div></div><div><h3>Conclusion</h3><div>This study revealed the chemical composition of XSHG and elucidated the great benefit of XSHG in the treatment of CTX combined with Acetylphenylhydrazine (APH)-induced BDS. This study explores the mechanism of XSHG from the perspective of JAK1/STAT1 signaling pathway for the first time, and provides a scientific basis for further study of XSHG and BDS.</div></div>","PeriodicalId":12147,"journal":{"name":"Fitoterapia","volume":"183 ","pages":"Article 106571"},"PeriodicalIF":2.5000,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fitoterapia","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0367326X25001960","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
引用次数: 0

Abstract

Background

As a classic prescription for postpartum diseases in traditional Chinese medicine prescriptions, Xin Sheng Hua Granule (XSHG) exerts pharmacological activities such as promoting blood circulation and removing blood stasis. However, its mechanism remains incompletely elucidated to date.

Purpose

To analyze the nascent particles by Ultra Performance Liquid Chromatography-Quadrupole-Time-of-Flight/Mass Spectrometry (UPLC-Q-TOF/MS), to explore the effectiveness of XSHG on blood deficiency syndrome, and to clarify its material basis and potential mechanism.

Methods

The chemical composition of nascent particles was qualitatively analyzed by UPLC-Q-TOF/MS. The mechanism of XSHG in alleviating blood deficiency syndrome was predicted using network pharmacology, and its effects were further investigated by establishing a rat model of blood deficiency. The expression of related proteins in the Janus Kinase 1 (JAK1)/ Signal Transducer and Activator of Transcription 1 (STAT1) signaling pathway and inflammatory proteins were examined using the methods such as Hematoxylin and Eosin (H&E), Real-Time Reverse Transcription PCR (qRT-PCR), Immunohistochemistry (IHC) and Western Blotting (WB) to elucidate the underlying protective mechanisms of XSHG in mitigating Blood Deficiency Syndrome (BDS).

Results

A total of 109 compounds were identified from the nascent particles. Network pharmacology research reveals that the mechanism of XSHG in the treatment of BDS may be related to the JAK1/STAT1 signaling pathway. In experiments, XSHG significantly protected mice against Cyclophosphamide (CTX) and APH-induced BDS by attenuating spleen histological changes and activities of Erythropoietin (EPO), (Granulocyte-Macrophage Colony-Stimulating Factor) GM-CSF. The BDS with CTX and APH-induced was inhibited by XSHG as confirmed by the inhibition of Tumor Necrosis Factor-alpha (TNF-α), Interleukin-1 beta (IL-1β) and Interleukin-6 (IL-6) production. Furthermore, CTX and APH-induced expression of JAK1 and STAT1, and activation of nuclear factor-κB (NF-κB) were significantly suppressed by XSHG.

Conclusion

This study revealed the chemical composition of XSHG and elucidated the great benefit of XSHG in the treatment of CTX combined with Acetylphenylhydrazine (APH)-induced BDS. This study explores the mechanism of XSHG from the perspective of JAK1/STAT1 signaling pathway for the first time, and provides a scientific basis for further study of XSHG and BDS.

Abstract Image

新生花颗粒通过抑制JAK1/STAT1通路激活改善化疗所致血虚证
新生花颗粒具有活血化瘀等药理作用,是中药方剂中治疗产后疾病的经典方剂。然而,其机制至今仍未完全阐明。目的采用超高效液相色谱-四极杆飞行时间/质谱(UPLC-Q-TOF/MS)对新生颗粒进行分析,探讨XSHG对血虚证的疗效,并阐明其物质基础和潜在机制。方法采用UPLC-Q-TOF/MS对新生颗粒的化学成分进行定性分析。采用网络药理学方法预测XSHG缓解血虚证的作用机制,并通过建立大鼠血虚模型进一步研究其作用。采用苏木精和伊红(H&;E)、实时反转录PCR (qRT-PCR)、免疫组化(IHC)和Western Blotting (WB)等方法检测Janus Kinase 1 (JAK1)/ Signal Transducer and Activator of Transcription 1 (STAT1)信号通路中相关蛋白和炎症蛋白的表达,以阐明XSHG减轻血虚综合征(BDS)的潜在保护机制。结果从初生颗粒中共鉴定出109个化合物。网络药理学研究表明,XSHG治疗BDS的机制可能与JAK1/STAT1信号通路有关。在实验中,XSHG通过降低脾脏组织学变化和红细胞生成素(EPO)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)的活性,显著保护小鼠免受环磷酰胺(CTX)和aph诱导的BDS。通过抑制肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)和白细胞介素-6 (IL-6)的产生,证实XSHG可抑制CTX和aph诱导的BDS。此外,XSHG显著抑制CTX和aph诱导的JAK1和STAT1的表达以及核因子-κB (NF-κB)的活化。结论本研究揭示了XSHG的化学成分,阐明了XSHG对CTX联合乙酰苯肼(Acetylphenylhydrazine, APH)诱导的BDS的治疗作用。本研究首次从JAK1/STAT1信号通路角度探讨了XSHG的作用机制,为进一步研究XSHG与BDS提供了科学依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Fitoterapia
Fitoterapia 医学-药学
CiteScore
5.80
自引率
2.90%
发文量
198
审稿时长
1.5 months
期刊介绍: Fitoterapia is a Journal dedicated to medicinal plants and to bioactive natural products of plant origin. It publishes original contributions in seven major areas: 1. Characterization of active ingredients of medicinal plants 2. Development of standardization method for bioactive plant extracts and natural products 3. Identification of bioactivity in plant extracts 4. Identification of targets and mechanism of activity of plant extracts 5. Production and genomic characterization of medicinal plants biomass 6. Chemistry and biochemistry of bioactive natural products of plant origin 7. Critical reviews of the historical, clinical and legal status of medicinal plants, and accounts on topical issues.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信