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Abstract

Study on the Mechanism of Kukoamine A Attenuating Interleukin-1 Beta Induced Chondrocyte Damage by Downregulating microRNA-302b-3p

Author(s): Yuntao Li, Zhaoli Wang*, Qi Zhang, Lin Shen, Yang Zhang and Yue Guo
Department of Integrated Traditional Chinese and Western Medicine ,Tianjin Hospital, 1Department of Orthopaedics, Integrated Traditional Chinese and Western Medicine, Tianjin Hospital, 2Department of Orthopaedics, Tianjin Hospital, 3Department of Tissue Engineering Research, Orthopaedic Research Institute of Tianjin Hospital, Tianjin 300211, China

Correspondence Address:
Zhaoli Wang, Department of Orthopaedics, Integrated Traditional Chinese and Western Medicine, Tianjin Hospital, Tianjin 300211, China, E-mail: liyuntao66552023@163.com


For probing the influence of kukoamine A on interleukin-1 beta-evoked damage of chondrocytes and its possible mechanism. Interleukin-1 beta was used to induce human knee joint chondrocytes to establish a cell injury model, and different concentrations of kukoamine A were used to treat chondrocytes. Following anti-microRNA-302b-3p introduction into chondrocytes, interleukin-1 beta (10 ng/ml) was employed for treating cells for 24 h. microRNA-NC and microRNA-302b-3p mimics were respectively transfected into chondrocytes and treated with kukoamine A (40 μmol/l) and interleukin-1 beta (10 ng/ml) for 24 h. Enzyme-linked immunosorbent assay method was used for detecting the levels of interleukin-6, tumour necrosis factor alpha, and interferon gamma. Flow cytometry was used for detecting the rate of cell apoptosis. The quantitative reverse transcription polymerase chain reaction was utilized for detecting microRNA-302b-3p level. Western blot was employed for detecting Bcl-2 associated X, apoptosis and B-cell lymphoma 2 protein levels. Kukoamine A could reduce interleukin-6, tumour necrosis factor alpha, and interferon gamma levels in chondrocytes induced by interleukin-1 beta, and could reduce the rate of apoptosis and the protein level of Bcl-2 associated X, apoptosis, and could also reduce the level of micoRNA-302b-3p, whereas it promoted B-cell lymphoma 2 level dose-dependently. After anti-microRNA-302b-3p introduction, interleukin-6, tumour necrosis factor alpha, and interferon gamma were downregulated, the rate of apoptosis and the protein level of Bcl-2 associated X, apoptosis were declined, whereas B-cell lymphoma 2 level was elevated. Transfection of microRNA-302b-3p mimics reversed kukoamine A impact on inflammation and apoptosis in interleukin-1 beta-evoked chondrocytes. Kukoamine A could inhibit cell inflammatory reaction and apoptosis by downregulating microRNA-302b-3p level, thereby reducing interleukin-1 beta induced chondrocyte damage.

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