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Original Research Article | OPEN ACCESS

Icariin induces autophagy and apoptosis of chondrocytes by inhibiting NF-?B signaling pathway

Jun Xiong, Hui Zou, Yi Yu

The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, PR China;

For correspondence:-  Yi Yu   Email: sp107e@163.com

Accepted: 25 August 2020        Published: 30 September 2020

Citation: Xiong J, Zou H, Yu Y. Icariin induces autophagy and apoptosis of chondrocytes by inhibiting NF-?B signaling pathway. Trop J Pharm Res 2020; 19(9):1851-1856 doi: 10.4314/tjpr.v19i9.8

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of icariin on autophagy and apoptosis of chondrocytes, and the associated mechanisms.
Methods: The chondrocytes were randomly divided into control (PBS intervention), TNF-α intervention, icarin +TNF-α, and NF-κB inhibition +TNF-α, with 8 strains in each group. The levels of IL-1, IL-6 and IL-12 were assayed by ELISA. The mRNA and protein expressions of ATG5, ATG7, Bax and Bcl-2 cells were determined by polymerase chain reaction (PCR) and Western blotting, while protein expressions of p-p65 and IκBα were assayed using Western blotting.
Results: In the cartilage tissue of rats in the icariin +TNF-α group and NF-κB inhibition +TNF-α group, IL-1, IL-6 and IL-12 levels were significantly lower than those in TNF-α treatment group (p < 0.05). The AATG5 mRNA and protein in cartilage tissues of rats in icariin +TNF-α and NF-κB inhibition +TNF-α groups were significantly higher than those in TNF-α group. Bax mRNA and protein in cartilage tissues of icariin +TNF-α and NF-κB inhibition +TNF-α groups were downregulated, relative to TNF-α group; on the other hand, Bcl-2 mRNA and protein were significantly higher than those of TNF-α group (p < 0.05). In the cartilage tissues of Icarin +TNF-α, NF-κB inhibition +TNF-α groups, P-p65 protein was significantly lower than that of TNF-α (p < 0.05).
Conclusion: TNF-α enhances the production of a large number of inflammatory factors by cartilage cells, inhibits autophagy of cartilage cells, and promotes cell apoptosis through regulation of NF-κB signaling pathway.

Keywords: Icariin, NF-κB signaling pathway, TNF-α, Inflammatory response, Chondrocytes, Autophagy, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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