Evidence map›Paper›PMID 32841225›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Dioscin Attenuates Interleukin 1β (IL-1β)-Induced Catabolism and Apoptosis via Modulating the Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling in Human Nucleus Pulposus Cells.

Longhui Wang, Yuntao Gu, Hai Zhao, Rong Chen, Wensheng Chen, Hao Qi, Weisong Gao

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Longhui WangDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Yuntao GuDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Hai ZhaoDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Rong ChenDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Wensheng ChenDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Hao QiDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Weisong GaoDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China (mainland).
Hainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Nucleus pulposus (NP) cell dysfunction and apoptosis contribute to disc degeneration. Dioscin, a natural steroid saponin, has been demonstrated to have anti-inflammatory, antiapoptotic, and antioxidative effects in various diseases. However, little is known about the roles of dioscin in intervertebral disc degeneration. MATERIAL AND METHODS To evaluate the roles of dioscin in disc degeneration and its specific mechanism, human NP cells were incubated with IL-1ß and various concentrations of dioscin. Cell viability, extracellular matrix protein expression, catabolic factors, degree of apoptosis, inflammatory factors, and related signaling pathways were evaluated by western blotting, fluorescence immunostaining, TUNEL staining, and reverse transcription PCR. RESULTS Dioscin inhibited IL-1ß-activated apoptotic signaling and catabolic activity in NP cells. Dioscin suppressed TLR4/NF-0kappaB signaling, and attenuated the level of inflammatory mediators (IL-6, TNF-alpha) in IL-1ß-stimulated human NP cells. CONCLUSIONS Our work provides the first evidence that dioscin attenuates IL-1ß-activated inflammation and catabolic activity in human NP cells through inhibiting the TLR4/NF-kappaB pathway, indicating that dioscin is a new potential candidate for clinical therapy to attenuate disc degeneration.

Indexed as

ApoptosisDiosgeninHumansInflammation MediatorsInterleukin-1betaNF-kappa BNucleus PulposusSignal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphadioscinDiosgeninIL1B protein, humanInflammation MediatorsInterleukin-1betaNF-kappa BTLR4 protein, humanToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID32841225
PMCPMC7466834
OpenAlexW3081171035

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.