Trans-Cinnamaldehyde Inhibits IL-1β-Stimulated Inflammation in Chondrocytes by Suppressing NF-κB and p38-JNK Pathways and Exerts Chondrocyte Protective Effects in a Rat Model of Osteoarthritis

Abstract

Objective. Trans-cinnamaldehyde (TCA), a compound from Cinnamomum cassia Presl, has been reported to have anti-inflammatory effect. However, its effect on cartilage degradation in osteoarthritis is unclear. This study is designed to examine the effects of TCA on cartilage in vitro and in vivo. Material and Methods. SW1353 cells and human primary chondrocytes were treated with varying concentrations of TCA (2-20 μg/ml) for 2 h followed by IL-1β stimulation. Cell viability was examined by the MTT assay. Expression of MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 was examined by Western blot and RT-qPCR. Monosodium iodoacetate (MIA)-induced OA was established in rats to assess the chondrocyte protective effects of intraperitoneal injection of TCA (50 mg/kg). Results. TCA at a concentration of 10 μg/ml had no significant effect on cell viability. MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 were decreased by TCA 2-10 μg/ml in a dose-dependent manner (all P<0.05). Pretreatment with TCA decreased the degradation of IκBα and increased the expression of p-IκBα, indicating that NF-κB inactivation was induced by TCA in IL-1β-stimulated SW1353 cells. Pretreatment with TCA decreased the levels of p-p38 and p-JNK, while the levels of p-ERK were not significantly affected. TCA 10 μg/ml significantly decreased expression levels of MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5. In vivo results showed that TCA alleviated cartilage destruction and the OARSI scores. Conclusion. TCA possesses anti-inflammatory effect in vitro and exerts chondrocyte protective effects in vivo, in which NF-κB and p38-JNK were involved.

Mangiferin alleviates experimental peri-implantitis via suppressing interleukin-6 production and Toll-like receptor 2 signaling pathway

“…P38 MAPK and JNK are important members of MAPK superfamily, which are implicated in regulating various inflammatory responses [44, 45]. Excessive phosphorylation of p38 MAPK and JNK has been reported in several inflammatory diseases, such as colitis and osteoarthritis, and the inhibition of the phosphorylation is correlated with the attenuation of inflammatory response [46, 47]. In recent research on a periodontitis-like environment, the overactivation of p38 MAPK and JNK was observed, and mangiferin treatment inhibited their activation and the production of proinflammatory cytokine in a dose-dependent manner [26].…”

COVID-19, cytokines, inflammation, and spices: How are they related?

“…Furthermore, it inhibits the activation of NF-κB as well as the degradation of IκB. It also slowed down the progression of osteoarthritis in vivo [ 252 ]. Suppression of NO due to a decrease in iNOS expression is also observed after TCA treatment in RAW 264.7 cells [ 253 ].…”

Inhibition effect of Caragana sinica root extracts on Osteoarthritis through MAPKs, NF-κB signaling pathway

“…Besides MMPs, cleavage of aggrecan can be mediated by several members of ADAMTS such as ADAMTS-4 and ADAMTS-5 in OA pathogenesis [46]. ADAMTS members play an important role in the degradation of proteoglycans and loss of GAGs [47]. Both ADAMTS-4 and ADAMTS-5 are key enzymes for cleaving aggrecans, but only ADAMTS-5 is active [48,49].…”