open access

Vol 58, No 4 (2020)
Original paper
Submitted: 2020-08-29
Accepted: 2020-10-20
Published online: 2020-10-29
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The protective impact of Trans-Cinnamaldehyde (TCA) against the IL-1b induced inflammation in in vitro osteoarthritis model by regulating PI3K/AKT pathways

Jian-rong Wu1, Wen-jie Zhong1, Zhen-dong Chen1, Ben-qi Zhu1, Yun-yun Jiang1, Piotr M. Wierzbicki2
DOI: 10.5603/FHC.a2020.0025
·
Pubmed: 33118610
·
Folia Histochem Cytobiol 2020;58(4):264-271.
Affiliations
  1. Department of Orthopedics, Zhejiang Greentown Cardiovascular Hospital, Hangzhou City, Zhejiang Province, China
  2. Department of Histology, Medical University of Gdansk, Gdansk, Poland

open access

Vol 58, No 4 (2020)
ORIGINAL PAPERS
Submitted: 2020-08-29
Accepted: 2020-10-20
Published online: 2020-10-29

Abstract

Introduction. Osteoarthritis (OA) is a severe joint degeneration disease in elderly people described by the advanced degradation of articular cartilage, which ultimately leads to chronic pain. Trans-cinnamaldehyde (TCA) exerted its anti-inflammatory function in numerous disease syndromes; however, its role in the pathogenesis of OA remains unknown. The current research aimed to explore the potential protective impact of TCA in the progression of osteoarthritis in vitro.

Material and methods. Human knee articular chondrocytes were treated with 10 ng/ml IL-1b alone for 24 h or in a combination in a pretreatment with TCA at different concentrations (2, 5, 10 μg/mL, 24 h). The viability and cell apoptosis were determined by CCK-8 assay and flow cytometry methods. The protein levels of IL-8, PGE2, and TNF-a and the levels of phosphorylated AKT and PI3K were evaluated using ELISA assay. Moreover, RT-qPCR was used to measure the relative mRNA expression of MMP-13, iNOS, COX-2, and ADAMTS-5 in IL-1b-induced chondrocytes.

Results. Our results revealed that the treatment with TCA had no effect on chondrocytes’ proliferation and apoptosis. Moreover, the protein levels of IL-8, TNF-a, and PGE2 were considerably reduced in IL-1b-induced chondrocytes treated with different concentrations of TCA. Furthermore, the mRNA expression of MMP-13, iNOS, COX-2, and ADAMTS-5 and the phosphorylation of AKT and PI3K were markedly reduced in IL-1b-induced chondrocytes with the increase in the concentration of TCA.

Conclusions. Trans-cinnamaldehyde inhibited the inflammation induced by IL-1b in chondrocytes through the PI3K/AKT pathway, which suggests that TCA might serve as a potential therapeutic agent for osteoarthritis treatment.

Abstract

Introduction. Osteoarthritis (OA) is a severe joint degeneration disease in elderly people described by the advanced degradation of articular cartilage, which ultimately leads to chronic pain. Trans-cinnamaldehyde (TCA) exerted its anti-inflammatory function in numerous disease syndromes; however, its role in the pathogenesis of OA remains unknown. The current research aimed to explore the potential protective impact of TCA in the progression of osteoarthritis in vitro.

Material and methods. Human knee articular chondrocytes were treated with 10 ng/ml IL-1b alone for 24 h or in a combination in a pretreatment with TCA at different concentrations (2, 5, 10 μg/mL, 24 h). The viability and cell apoptosis were determined by CCK-8 assay and flow cytometry methods. The protein levels of IL-8, PGE2, and TNF-a and the levels of phosphorylated AKT and PI3K were evaluated using ELISA assay. Moreover, RT-qPCR was used to measure the relative mRNA expression of MMP-13, iNOS, COX-2, and ADAMTS-5 in IL-1b-induced chondrocytes.

Results. Our results revealed that the treatment with TCA had no effect on chondrocytes’ proliferation and apoptosis. Moreover, the protein levels of IL-8, TNF-a, and PGE2 were considerably reduced in IL-1b-induced chondrocytes treated with different concentrations of TCA. Furthermore, the mRNA expression of MMP-13, iNOS, COX-2, and ADAMTS-5 and the phosphorylation of AKT and PI3K were markedly reduced in IL-1b-induced chondrocytes with the increase in the concentration of TCA.

Conclusions. Trans-cinnamaldehyde inhibited the inflammation induced by IL-1b in chondrocytes through the PI3K/AKT pathway, which suggests that TCA might serve as a potential therapeutic agent for osteoarthritis treatment.

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Keywords

human articular chondrocytes; IL-1b; osteoarthritis model; trans-cinnamaldehyde; PI3K/AKT pathway; RT-qPCR; ELISA

About this article
Title

The protective impact of Trans-Cinnamaldehyde (TCA) against the IL-1b induced inflammation in in vitro osteoarthritis model by regulating PI3K/AKT pathways

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 58, No 4 (2020)

Article type

Original paper

Pages

264-271

Published online

2020-10-29

DOI

10.5603/FHC.a2020.0025

Pubmed

33118610

Bibliographic record

Folia Histochem Cytobiol 2020;58(4):264-271.

Keywords

human articular chondrocytes
IL-1b
osteoarthritis model
trans-cinnamaldehyde
PI3K/AKT pathway
RT-qPCR
ELISA

Authors

Jian-rong Wu
Wen-jie Zhong
Zhen-dong Chen
Ben-qi Zhu
Yun-yun Jiang
Piotr M. Wierzbicki

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