Corilagin attenuates osteoarthritis progression by coordinating NF-κB inhibition with PI3K/AKT/mTOR-associated autophagy restoration.

Zhou R, Li Jie, Chen S, Meng C, Liu Q, Huang X, You H · 2026 · International Immunopharmacology · Atlas ID ZHOU2026B

What this study shows

Corilagin restores chondrocyte autophagic flux and ECM synthesis by inhibiting PI3K/AKT/mTOR and NF-κB signalling, reducing cartilage erosion and OARSI scores in the mouse DMM osteoarthritis model.

Abstract

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Osteoarthritis (OA) is characterized by persistent inflammation, extracellular matrix degradation and impaired autophagy. IL-1β-stimulated primary mouse chondrocytes were used to evaluate Corilagin. Corilagin restored chondrocyte proliferation and increased Aggrecan, collagen II and SOX9 expression while reducing MMP3, MMP13, iNOS and COX2. Mechanistically, Corilagin inhibited PI3K/AKT/mTOR and NF-κB signaling, reduced p65 nuclear translocation and restored autophagic flux (increased Beclin-1 and LC3 II/I, decreased p62). 3-MA partially abolished these protective effects.

Read the full abstract on PubMed →

At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (DMM OA model); primary mouse chondrocytes); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Mouse (DMM OA model); primary mouse chondrocytes
Journal	International Immunopharmacology
Year	2026
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1016/j.intimp.2026.117342 · PMID 42664894

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	Corilagin (intra-articular)
Target	PI3K/AKT/mTOR; NF-κB; autophagy (Beclin-1, LC3, p62)
Model	Mouse
Effect	Restored autophagic flux, suppressed catabolic and inflammatory markers, protected cartilage in vivo

In the Atlas

Cite this paper

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Zhou, R., Li Jie, Chen, S., Meng, C., Liu, Q., Huang, X., & You, H. (2026). Corilagin attenuates osteoarthritis progression by coordinating NF-κB inhibition with PI3K/AKT/mTOR-associated autophagy restoration. International Immunopharmacology. https://doi.org/10.1016/j.intimp.2026.117342

@article{ZHOU2026B,
  author       = {Zhou, R. and Li Jie and Chen, S. and Meng, C. and Liu, Q. and Huang, X. and You, H.},
  title        = {{Corilagin attenuates osteoarthritis progression by coordinating NF-κB inhibition with PI3K/AKT/mTOR-associated autophagy restoration}},
  journal      = {International Immunopharmacology},
  year         = {2026},
  doi          = {10.1016/j.intimp.2026.117342},
  note         = {PMID: 42664894},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record ZHOU2026B) [Data set]. https://mtor-atlas.org/study/ZHOU2026B/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_ZHOU2026B,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record ZHOU2026B},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/ZHOU2026B/},
  doi          = {10.5281/zenodo.22059963}
}

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