Evidence map›Paper›PMID 35965964›Full record

ArticleDrug design, development and therapy2022

Corosolic Acid Protects Rat Chondrocytes Against IL-1β-Induced ECM Degradation by Activating Autophagy via PI3K/AKT/mTOR Pathway and Ameliorates Rat Osteoarthritis.

Hui Han, Ming Chen, Zhenyu Li, Siqi Zhou, Yingbin Wu, Jian Wei

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
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  8. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    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

6 authors at 4 institutions in 1 country.

Hui Han *Department of Sports Medicine and Joint Orthopedics, Liuzhou People's Hospital, Liuzhou, Guangxi, People's Republic of China.
Ming Chen *Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, People's Republic of China.
Zhenyu Li *Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, People's Republic of China.
Siqi ZhouDepartment of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, People's Republic of China.
Yingbin WuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, People's Republic of China.
Jian WeiDepartment of Sports Medicine and Joint Orthopedics, Liuzhou People's Hospital, Liuzhou, Guangxi, People's Republic of China.
Liuzhou General Hospital · CNWuhan University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Osteoarthritis (OA) is an age-related degenerative disease associated with enhanced degradation of extracellular matrix (ECM) and decreased autophagy. Our study is aimed to explore how corosolic acid (CRA) affect cartilage ECM metabolism and the potential mechanism. Methods: Rat chondrocytes were pretreated with different concentrations of CRA (0, 2.5, 5, and 10 μM), and were stimulated with IL-1β (10ng/mL) for 24 h, subsequently. RT-qPCR, Western blot, and immunofluorescence were used to detect the expression of genes related to ECM metabolism and explore the potential molecular mechanism. The effect of CRA on articular cartilage was observed in the surgically induced OA rat model with the method of Safranin O/Fast green and immunohistochemical staining. Results: Results showed that CRA reversed the IL-1β-induced degradation of aggrecan and type II collagen and the high expression of MMP13 and ADAMTS5. Mechanistically, CRA enhanced autophagy through inhibiting the classical PI3K/AKT/mTOR signaling pathway. Furthermore, inhibition of autophagy partly abolished the protective effects of CRA on ECM synthesis in IL-1β-treated chondrocytes. Correspondingly, the protective effect of CRA was also confirmed in a rat OA model. Conclusion: Herein, we demonstrate that CRA can enhance autophagy by inhibiting PI3K/AKT/mTOR signaling pathway, prevent IL-1β-induced cartilage ECM degradation, and may be a potentially applicable candidate for the treatment of OA.

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsAutophagyChondrocytesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsTOR Serine-Threonine KinasesTriterpenescorosolic acidmTOR protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTriterpenesautophagycorosolic acidextracellular matrixosteoarthritisPI3K/AKT/mTOR signaling

Identifiers

PMID35965964
PMCPMC9364989
OpenAlexW4289979052

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.