Evidence map›Paper›PMID 42453001›Full record

ArticleInternational journal of rheumatic diseases2026

JAK Inhibitor Tofacitinib Ameliorates Inflammation Response and Osteogenic Differentiation in Immune-Mediated Inflammatory Arthritis in Rats.

Zhiming Zhang, Zhiming Lin, Genlian Hu, Qingqing Huang, Congrong Xu, Jiafang Zhang, Fangzhen Wu, Rongbin Song, Hongshan Chen, Feng Zheng

Abstract read
In one paragraph

Article in International journal of rheumatic diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Zhiming ZhangDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Zhiming LinDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Genlian HuDepartment of Preventive Treatment of Disease, The Third People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
Qingqing HuangDepartment of Rheumatology and Immunology, Sanming Integrated Traditional Chinese and Western Medicine Hospital, Sanming, Fujian, China.
Congrong XuDepartment of Clinical Laboratory Medicine, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Jiafang ZhangDepartment of Spinal Surgery, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Fangzhen WuDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Rongbin SongDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Hongshan ChenDepartment of Clinical Laboratory Medicine, The Second Affiliated Hospital of Fujian Traditional Chinese Medical University, Fuzhou, Fujian, China.
Feng ZhengDepartment of Rheumatology and Immunology, Fuzhou Second General Hospital, Fuzhou, Fujian, China.ORCID https://orcid.org/0009-0000-2902-8240

Funding

Fujian Provincial Education Research Project for Young and Middle-aged Teachers (Science and Technology) JAT200226Fujian Provincial Natural Science Foundation Project 2023J011523Guangzhou Science and Technology Program Key Project 2023B03J1244
6 · The paper itself

Abstract

objectiveThis study sought to investigate the mechanism by which tofacitinib affects inflammatory response and osteogenic differentiation in immune-mediated inflammatory arthritis in rats in relation to Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3).

methodsWistar male rats were induced by the combination of bovine proteoglycan and incomplete/complete Freund's adjuvant to establish the immune-mediated inflammatory arthritis model. The clinical manifestations were observed. Hematoxylin and eosin staining was used to evaluate pathological changes in sacroiliac joints and surrounding cartilage. Additionally, the levels of osteogenic differentiation-related proteins, serum inflammatory factors, and alkaline phosphatase (ALP) were measured. Flow cytometry was conducted to analyze the proportion of Th17 cells in peripheral blood. Alizarin red staining detected the osteogenic differentiation of ligament fibroblasts.

resultsThe rats exhibited joint swelling, inflammatory infiltration in the sacroiliac joint, and cartilage destruction after modeling. Elevations were also detected in the levels of serum pro-inflammatory factors, the proportion of Th17 cells, ALP activity, phosphorylated (p)-JAK1/2, p-STAT3, osteogenic differentiation markers in ligament fibroblasts, as well as in the mineralized nodules. Tofacitinib intervention inhibited the phosphorylation of JAK and STAT3, downregulated bone differentiation-related proteins, decreased the mineralized nodules, reduced the activity of ALP, and decreased the levels of pro-inflammatory factors. However, the combined use of the STAT3 agonist Colivelin partially reversed the inhibitory effect of tofacitinib on joint inflammation and osteogenic differentiation.

conclusionTofacitinib alleviated the inflammatory response in immune-mediated inflammatory arthritis and inhibited osteogenic differentiation in rats via inhibition of the JAK/STAT3 signaling pathway.

Indexed as

Anti-Inflammatory AgentsArthritis, ExperimentalCell DifferentiationJanus Kinase InhibitorsJanus KinasesOsteogenesisPiperidinesPyrimidinesSacroiliac JointAnimalsCytokinesInflammation MediatorsMalePhosphorylationPyrrolesRats, WistarAnti-Inflammatory AgentsCytokinesInflammation MediatorsJanus Kinase InhibitorsJanus KinasesPiperidinesPyrimidinesPyrrolesStat3 protein, ratSTAT3 Transcription Factortofacitinibinflammatory disorderinflammatory responseJAK/STAT3 signaling pathwayosteogenic differentiationtofacitinib

Identifiers

PMID42453001
PMCPMC13370143

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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.