Carthamus tinctorius L. inhibits hepatic fibrosis and hepatic stellate cell activation by targeting the PI3K/Akt/mTOR pathway.

IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Molecular medicine reports Pub Date : 2024-11-01 Epub Date: 2024-09-02 DOI:10.3892/mmr.2024.13314
Zhiheng Dong, Haibin Guan, Lu Wang, Lijuan Liang, Yifan Zang, Lan Wu, Lidao Bao
{"title":"<i>Carthamus tinctorius</i> <i>L.</i> inhibits hepatic fibrosis and hepatic stellate cell activation by targeting the PI3K/Akt/mTOR pathway.","authors":"Zhiheng Dong, Haibin Guan, Lu Wang, Lijuan Liang, Yifan Zang, Lan Wu, Lidao Bao","doi":"10.3892/mmr.2024.13314","DOIUrl":null,"url":null,"abstract":"<p><p>Hepatic fibrosis (HF) is a process that occurs during the progression of several chronic liver diseases, for which there is a lack of effective treatment options. <i>Carthamus tinctorius L.</i> (CTL) is often used in Chinese or Mongolian medicine to treat liver diseases. However, its mechanism of action remains unclear. In the present study, CTL was used to treat rats with CCl4‑induced HF. The histopathological, biochemical and HF markers of the livers of the rats were analyzed, and CTL‑infused serum was used to treat hepatic stellate cells (HSCs) in order to detect the relevant markers of HSC activation. Protein expression pathways were detected both <i>in vitro</i> and <i>in vivo</i>. Histopathological results showed that CTL significantly improved CCl4‑induced liver injury, reduced aspartate aminotransferase and alanine aminotransferase levels, promoted E‑cadherin expression, and decreased α‑smooth muscle actin (SMA), SOX9, collagen I and hydroxyproline expression. Moreover, CTL‑infused serum was found to decrease α‑SMA and collagen I expression in HSCs. Further studies showed that CTL inhibited the activity of the PI3K/Akt/mTOR pathway in the rat livers. Following the administration of the PI3K agonist 740Y‑P to HSCs, the inhibitory effect of CTL on the PI3K/Akt//mTOR pathway was blocked. These results suggested that CTL can inhibit HF and HSC activation by inhibiting the PI3K/Akt/mTOR pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391516/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular medicine reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/mmr.2024.13314","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/2 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Hepatic fibrosis (HF) is a process that occurs during the progression of several chronic liver diseases, for which there is a lack of effective treatment options. Carthamus tinctorius L. (CTL) is often used in Chinese or Mongolian medicine to treat liver diseases. However, its mechanism of action remains unclear. In the present study, CTL was used to treat rats with CCl4‑induced HF. The histopathological, biochemical and HF markers of the livers of the rats were analyzed, and CTL‑infused serum was used to treat hepatic stellate cells (HSCs) in order to detect the relevant markers of HSC activation. Protein expression pathways were detected both in vitro and in vivo. Histopathological results showed that CTL significantly improved CCl4‑induced liver injury, reduced aspartate aminotransferase and alanine aminotransferase levels, promoted E‑cadherin expression, and decreased α‑smooth muscle actin (SMA), SOX9, collagen I and hydroxyproline expression. Moreover, CTL‑infused serum was found to decrease α‑SMA and collagen I expression in HSCs. Further studies showed that CTL inhibited the activity of the PI3K/Akt/mTOR pathway in the rat livers. Following the administration of the PI3K agonist 740Y‑P to HSCs, the inhibitory effect of CTL on the PI3K/Akt//mTOR pathway was blocked. These results suggested that CTL can inhibit HF and HSC activation by inhibiting the PI3K/Akt/mTOR pathway.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
通过靶向 PI3K/Akt/mTOR 通路抑制肝纤维化和肝星状细胞活化
肝纤维化(HF)是几种慢性肝病进展过程中出现的一个过程,目前尚缺乏有效的治疗方案。中药或蒙药中经常使用麝香草苷(CTL)来治疗肝病。然而,其作用机制仍不清楚。在本研究中,CTL 被用于治疗 CCl4 诱导的高频肝病大鼠。研究分析了大鼠肝脏的组织病理学、生化和高频标志物,并用CTL注入的血清治疗肝星状细胞(HSCs),以检测HSC活化的相关标志物。检测了体外和体内的蛋白质表达途径。组织病理学结果显示,CTL能明显改善CCl4诱导的肝损伤,降低天冬氨酸氨基转移酶和丙氨酸氨基转移酶水平,促进E-cadherin的表达,降低α-平滑肌肌动蛋白(SMA)、SOX9、胶原蛋白I和羟脯氨酸的表达。此外,还发现注入 CTL 的血清可降低造血干细胞中 α-SMA 和胶原 I 的表达。进一步的研究表明,CTL 可抑制大鼠肝脏中 PI3K/Akt/mTOR 通路的活性。给造血干细胞注射PI3K激动剂740Y-P后,CTL对PI3K/Akt//mTOR通路的抑制作用被阻断。这些结果表明,CTL可通过抑制PI3K/Akt/mTOR途径来抑制高频和造血干细胞的活化。
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 去求助
来源期刊
Molecular medicine reports
Molecular medicine reports 医学-病理学
CiteScore
7.60
自引率
0.00%
发文量
321
审稿时长
1.5 months
期刊介绍: Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
期刊最新文献
[Corrigendum] MicroRNA‑378 enhances migration and invasion in cervical cancer by directly targeting autophagy‑related protein 12. [Retracted] Carnosol inhibits osteoclastogenesis in vivo and in vitro by blocking the RANKL‑induced NF‑κB signaling pathway. Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review). Orphan nuclear receptor NR4A1 regulates both osteoblastogenesis and adipogenesis in human mesenchymal stem cells. [Retracted] Molecular mechanism of atractylon in the invasion and migration of hepatic cancer cells based on high‑throughput sequencing.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1