Notoginsenoside Fc alleviates oxidized low-density lipoprotein-induced endothelial cell dysfunction and upregulates PPAR-γ in vitro.

IF 2.5 4区 生物学 Q3 CELL BIOLOGY Histology and histopathology Pub Date : 2024-07-01 Epub Date: 2023-12-20 DOI:10.14670/HH-18-694
Yuanhao Zhang, Kui Liu, Dile Wang
{"title":"Notoginsenoside Fc alleviates oxidized low-density lipoprotein-induced endothelial cell dysfunction and upregulates PPAR-γ <i>in vitro</i>.","authors":"Yuanhao Zhang, Kui Liu, Dile Wang","doi":"10.14670/HH-18-694","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Deep venous thrombosis (DVT) is a prevalent vascular disease and a major cause of morbidity and mortality worldwide. Notoginsenoside Fc (NFc) is a protopanaxadiol-type saponin that has been shown to have beneficial effects on several disorders. However, its function in DVT is unclear.</p><p><strong>Methods: </strong>Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic DVT <i>in vitro</i> and treated with NFc to investigate its functions. CCK-8 assay was utilized for measuring cell viability. Western blotting was used for detecting protein levels of proinflammatory cytokines, apoptosis-related markers, and peroxisome proliferator-activated receptor-γ (PPAR-γ). Flow cytometry was performed for cell apoptosis detection. Levels of oxidative stress-related markers were examined by the DCFH-DA method and ELISA. RT-qPCR was utilized for the measurement of PPAR-γ mRNA level.</p><p><strong>Results: </strong>NFc increased the viability and suppressed inflammation, apoptosis, and oxidative stress in ox-LDL-treated HUVECs. NFc treatment induced upregulation of PPAR-γ in HUVECs.</p><p><strong>Conclusion: </strong>NFc mitigates ox-LDL-induced dysfunction of HUVECs.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Histology and histopathology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.14670/HH-18-694","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/20 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Deep venous thrombosis (DVT) is a prevalent vascular disease and a major cause of morbidity and mortality worldwide. Notoginsenoside Fc (NFc) is a protopanaxadiol-type saponin that has been shown to have beneficial effects on several disorders. However, its function in DVT is unclear.

Methods: Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic DVT in vitro and treated with NFc to investigate its functions. CCK-8 assay was utilized for measuring cell viability. Western blotting was used for detecting protein levels of proinflammatory cytokines, apoptosis-related markers, and peroxisome proliferator-activated receptor-γ (PPAR-γ). Flow cytometry was performed for cell apoptosis detection. Levels of oxidative stress-related markers were examined by the DCFH-DA method and ELISA. RT-qPCR was utilized for the measurement of PPAR-γ mRNA level.

Results: NFc increased the viability and suppressed inflammation, apoptosis, and oxidative stress in ox-LDL-treated HUVECs. NFc treatment induced upregulation of PPAR-γ in HUVECs.

Conclusion: NFc mitigates ox-LDL-induced dysfunction of HUVECs.

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
Notoginsenoside Fc能缓解氧化低密度脂蛋白诱导的内皮细胞功能障碍,并在体外上调PPAR-γ。
背景:深静脉血栓(DVT)是一种常见的血管疾病,也是全球发病率和死亡率的主要原因。野葛根皂甙 Fc(NFc)是一种原人参二醇型皂甙,已被证明对多种疾病有益处。方法:用氧化低密度脂蛋白(ox-LDL)处理人脐静脉内皮细胞(HUVECs)以模拟体外深静脉血栓,并用 NFc 处理以研究其功能。CCK-8测定法用于测量细胞活力。用 Western 印迹法检测促炎细胞因子、细胞凋亡相关标志物和过氧化物酶体增殖激活受体-γ(PPAR-γ)的蛋白水平。流式细胞术用于检测细胞凋亡。用 DCFH-DA 法和酶联免疫吸附法检测氧化应激相关标记物的水平。利用 RT-qPCR 检测 PPAR-γ mRNA 水平:结果:NFc 提高了氧化-LDL 处理的 HUVECs 的活力,抑制了炎症、细胞凋亡和氧化应激。结果:NFc 提高了氧化-LDL 处理的 HUVEC 的活力,抑制了炎症凋亡和氧化应激,NFc 处理诱导了 HUVEC 中 PPAR-γ 的上调:结论:NFc 可减轻氧化-LDL 诱导的 HUVECs 功能障碍。
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
Histology and histopathology
Histology and histopathology 生物-病理学
CiteScore
3.90
自引率
0.00%
发文量
232
审稿时长
2 months
期刊介绍: HISTOLOGY AND HISTOPATHOLOGY is a peer-reviewed international journal, the purpose of which is to publish original and review articles in all fields of the microscopical morphology, cell biology and tissue engineering; high quality is the overall consideration. Its format is the standard international size of 21 x 27.7 cm. One volume is published every year (more than 1,300 pages, approximately 90 original works and 40 reviews). Each volume consists of 12 numbers published monthly online. The printed version of the journal includes 4 books every year; each of them compiles 3 numbers previously published online.
期刊最新文献
Correlation of NAT10 expression with clinical data and survival profiles in esophageal squamous cell carcinoma patients, and its impact on cell proliferation and apoptosis. Qualitative evaluations of reactive microglial heterogeneity in cultured porcine retina. S100A2 upregulates GLUT1 expression to promote glycolysis in the progression of nasopharyngeal carcinoma. Oridonin alleviates inflammation and endoplasmic reticulum stress in pediatric pneumonia via regulating the SIRT1-mediated Wnt/β-catenin signaling pathway. Brain endothelial cell activation and dysfunction associate with and contribute to the development of enlarged perivascular spaces and cerebral small vessel disease.
×
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