Evidence map›Paper›PMID 32525787›Full record

ArticleCurrent molecular pharmacology2021

Nuezhenide Exerts Anti-Inflammatory Activity through the NF-κB Pathway.

Qin-Qin Wang, Shan Han, Xin-Xing Li, Renyikun Yuan, Youqiong Zhuo, Xinxin Chen, Chenwei Zhang, Yangling Chen, Hongwei Gao, Li-Chun Zhao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Current molecular pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Effect ofAnimal biotechnology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Foods (Basel, Switzerland) · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Qin-Qin WangCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Shan HanCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Xin-Xing LiCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Renyikun YuanState Key Laboratory of Innovative Drug and Efficient Energy-Saving Pharmaceutical Equipment, Jiangxi University of Traditional Chinese Medicine, Nanchang 330004, China.
Youqiong ZhuoCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Xinxin ChenCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Chenwei ZhangCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Yangling ChenCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Hongwei GaoCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Li-Chun ZhaoCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Shilin YangCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China.
Guangxi University · CNJiangxi University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNuezhenide (NZD), an iridoid glycoside isolated from Ilex pubescens Hook. & Arn. var. kwangsiensis Hand.-Mazz., used as a traditional Chinese medicine for clearing away heat and toxic materials, displays a variety of biological activities such as anti-tumor, antioxidant, and other life-protecting activities. However, a few studies involving anti-inflammatory activity and the mechanism of NZD have also been reported. In the present study, the anti-inflammatory and antioxidative effects of NZD are illustrated.

objectiveThis study aims to test the hypothesis that NZD suppresses LPS-induced inflammation by targeting the NF-κB pathway in RAW264.7 cells.

methodsLPS-stimulated RAW264.7 cells were employed to detect the effect of NZD on the release of cytokines by ELISA. Protein expression levels of related molecular markers were quantitated by western blot analysis. The levels of ROS, NO, and Ca2+ were detected by flow cytometry. The changes in mitochondrial reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were observed and verified by fluorescence microscopy. Using immunofluorescence assay, the translocation of NF-κB/p65 from the cytoplasm into the nucleus was determined by confocal microscopy.

resultsNZD exhibited anti-inflammatory activity and reduced the release of inflammatory cytokines such as nitrite, TNF-α, and IL-6. NZD suppressed the expression of the phosphorylated proteins like IKKα/β, IκBα, and p65. Besides, the flow cytometry results indicated that NZD inhibited the levels of ROS, NO, and Ca2+ in LPS-stimulated RAW264.7 cells. JC-1 assay data showed that NZD reversed LPS-induced MMP loss. Furthermore, NZD suppressed LPS-induced NF-B/p65 translocation from the cytoplasm into the nucleus.

conclusionNZD exhibits anti-inflammatory effects through the NF-κB pathway on RAW264.7 cells.

Indexed as

AnimalsAnti-Inflammatory AgentsCell SurvivalCytokinesGlucosidesHumansInterleukin-6Membrane Potential, MitochondrialMiceNF-KappaB Inhibitor alphaNitric OxideNitritesPyransRAW 264.7 CellsReactive Oxygen SpeciesSignal TransductionAnti-Inflammatory AgentsCytokinesGlucosidesInterleukin-6NF-KappaB Inhibitor alphaNitric OxideNitritesnuezhenidePyransReactive Oxygen SpeciesTranscription Factor RelATumor Necrosis Factor-alphaanti-inflammationcytotoxicityLPSNF-κB pathwayNuezhenideRAW264.7 cells

Identifiers

PMID32525787
PMCPMC8778660
OpenAlexW3034640545

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.