Evidence map›Paper›PMID 36439628›Full record

ArticleJournal of orthopaedic translation2023

Stevioside attenuates osteoarthritis via regulating Nrf2/HO-1/NF-κB pathway.

Jia Wu, Haoliang Li, Fei Hu, Peng Luo

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic translation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. ALDH1L1 reverses CD8Journal of translational medicine · 2026
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  11. Advancing Nanomedicine: For Bone Defect Repair and Regeneration.International journal of nanomedicine · 2025
    Review
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  19. 2023 January issue Journal of Orthopaedic Translation.Journal of orthopaedic translation · 2023
    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

4 authors at 2 institutions in 1 country.

Jia WuKey Laboratory for Laboratory Medicine, Ministry of Education, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Science, WenzhouMedical University, Wenzhou, Zhejiang, 325035, China.
Haoliang LiDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xue Yuan Xi Road, Wenzhou, Zhejiang, 325000, China.
Fei HuDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xue Yuan Xi Road, Wenzhou, Zhejiang, 325000, China.
Peng LuoDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xue Yuan Xi Road, Wenzhou, Zhejiang, 325000, China.
Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Osteoarthritis (OA) is a chronic disease that may cause articular cartilage degeneration, and synovial inflammation, resulting in considerable pain, poor quality of life, and functional limitations. Previous research has shown that ECM degradation and inflammation are involved in the progression of OA. Stevioside (STE), a naturally diterpenoid glycoside, is isolated from the Methods: In the present study, we examined the anti-inflammatory effects of STE (STE) in both mouse chondrocytes and OA model induced by destabilization of the medial meniscus (DMM). Results: STE remarkably inhibited the IL-1β-induced expression of iNOS and Cox-2, generation of MMP-13, ADAMTS-4 and degradation of Aggrecan and Collagen II. Furthermore, we found that the chondroprotective effect of STE via Nrf2/HO-1/NF-κB signaling pathway. In vivo, the cartilage treated with STE displayed attenuated degeneration, low OARIS scores compared with DMM group. In conclusion, we considered that STE might be a promising therapeutic agent for the treatment of OA in future. Conclusions: Our findings indicated that STE can ameliorate the development of OA via inhibiting the inflammation. The underlying mechanism may be related to the Nrf2/HO-1/NF-κB signaling pathway. Moreover, the treatment of STE significantly relieves the progression in the mouse DMM model. All of the results demonstrated the therapeutic of STE in OA treatment. The translational potential of this article: This study demonstrates a more efficient and safe application of STE in treating osteoarthritis, provide a new concept for the cartilage targeted application of natural compounds.

Indexed as

Anti-inflammationNrf2/HO-1/NF-κB signaling pathwayOsteoarthritisPotential agentStevioside

Identifiers

PMID36439628
PMCPMC9674883
OpenAlexW4309107128

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.