ArticleCytotechnology2016
Naringin inhibits lipopolysaccharide-induced damage in human umbilical vein endothelial cells via attenuation of inflammation, apoptosis and MAPK pathways.
Article in Cytotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- The Effects of Naringin on Antioxidant Function, Intestinal Barrier and Immune Response in Broilers Challenged with Lipopolysaccharide.Animals : an open access journal from MDPI · 2025Article
- COVID-19-Associated Sepsis: Potential Role of Phytochemicals as Functional Foods and Nutraceuticals.International journal of molecular sciences · 2024Review
- Exploring the Therapeutic Effects ofNutrients · 2024Article
- Role of naringin in the treatment of atherosclerosis.Frontiers in pharmacology · 2024Review
- Naringin inhibits P2X4 receptor expression on satellite glial cells in the neonatal rat dorsal root ganglion.Journal of applied biomedicine · 2023Article
- Citrus flavonoids and adhesion molecules: Potential role in the management of atherosclerosis.Heliyon · 2023Review
- Review
- Review
- Naringin protects endothelial cells from apoptosis and inflammation by regulating the Hippo-YAP Pathway.Bioscience reports · 2020Article
- 4'-O-β-D-glucosyl-5-O-methylvisamminol ameliorates imiquimod-induced psoriasis-like dermatitis and inhibits inflammatory cytokines production by suppressing the NF-κB and MAPK signaling pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- The inhibition of Bax activation-induced apoptosis by RasGRP2 via R-Ras-PI3K-Akt signaling pathway in the endothelial cells.Scientific reports · 2019Article
- 5,2'-dibromo-2,4',5'-trihydroxydiphenylmethanone attenuates LPS-induced inflammation and ROS production in EA.hy926 cells via HMBOX1 induction.Journal of cellular and molecular medicine · 2019Article
- Apigenin reduces the Toll-like receptor-4-dependent activation of NF-κB by suppressing the Akt, mTOR, JNK, and p38-MAPK.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS.Molecules (Basel, Switzerland) · 2017Article
- Notoginsenoside R1 protects human keratinocytes HaCaT from LPS-induced inflammatory injury by downregulation of Myd88.International journal of immunopathology and pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial cell activation, injury and dysfunction have been regarded as one of the initial key events in the pathogenesis of atherosclerosis. Lipopolysaccharide (LPS), an important mediator of inflammation, can cause endothelial cell damage and apoptosis. Naringin (Nar), one major flavanone glycoside from citrus fruits, shows various pharmacological actions, but the effect of Nar on LPS-induced damage in human umbilical vein endothelial cells (HUVECs) remains unknown. The present results showed that Nar significantly improved the survival rate of HUVECs, and decreased reactive oxygen species and intracellular Ca(2+) levels caused by LPS compared with model group. In addition, Nar obviously decreased cytochrome c release from mitochondria into cytosol. Moreover, Nar significantly down-regulated the protein or mRNA levels of IL-1, IL-6, TNF-α, VCAM-1, ICAM-1, NF-κB, AP-1, cleaved-3,-7,-9, p53, Bak and Bax, and up-regulated the expressions of Bcl-xl, Bcl-2 to suppress inflammation and apoptosis. Furthermore, Nar obviously inhibited phosphorylation levels of JNK, ERK and p38 MAPK. In conclusion, Nar exhibited potent effects against LPS-induced damage in HUVECs through the modulation of oxidative stress, inflammation, apoptosis and MAPK pathways, which should be developed as a potent candidate for the treatment of atherosclerosis in the future.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.