Naringin in repairing articular cartilage injury by activating TGF-β/Smad signaling pathway to attenuate inflammatory response

Abstract

Naringin protects cartilage and attenuates inflammation. This study investigated the mechanism by which naringin activates the TGF-β/Smad signaling pathway to attenuate the inflammatory response and repair rabbit articular cartilage injury. A ring bone extraction drill was used to create a rabbit articular cartilage injury model. Sixteen Japanese white rabbits were divided into Sham, Mod, Nar, and Con groups and treated for 12 weeks. Compared with the Mod group, obvious signs of morphological and structural repair of cartilage injury were observed in the Nar group. The ICRS, BV/TV, and BS/TV scores increased, whereas the Wakitani and Tb.Sp scores decreased. Furthermore, ADAMTS-5 levels were significantly reduced, and TGF-β1 levels were significantly increased. The average light density of P-Smad3 in the repaired tissue was significantly elevated, whereas that of MMP-13 was significantly reduced. Compared with that in the Sham group, the transcription and expression levels of TβRII, type II collagen, P-TβRII, and P-Smad2 in the repair tissues of the Mod group were lower. This was reversed in the Nar group. Therefore, naringin administration can improve the morphology and structure of articular cartilage injury, reduce the concentration and expression levels of pro-inflammatory factors in the joint fluid and repair tissues, and increase the concentrations and expression levels of anti-inflammatory factors in the joint fluid and repair tissues. Thus, naringin exerts a positive effect by reducing the inflammatory response and repairing articular cartilage injury. This mechanism is closely related to the activation of the TGF-β/Smad signaling pathway.