Abstract
Osteoarthritis (OA) is a chronic degenerative disease featured by cartilage erosion and inflammation. Luteolin, a member of the flavonoid family, has been shown to exert anti-inflammatory and antioxidative activities. However, the potential biological effects and underlying mechanism of luteolin on chondrocytes and OA progression remain largely elusive. In this study, the potential effect and mechanism of luteolin on OA were investigated in vitro and in vivo. Our data revealed that luteolin inhibited H2O2-induced cell death, apoptosis, oxidative stress, programmed necrosis, and inflammatory mediator production in primary murine chondrocytes. In addition, luteolin could activate the AMPK and Nrf2 pathways, and AMPK serves as a positive upstream regulator of Nrf2. In vivo results demonstrated the therapeutic effects of luteolin on OA in the DMM mouse model. Collectively, our findings showed that luteolin might serve as a novel and effective treatment for OA and provided a new research direction for clinical OA therapies.
Highlights
Osteoarthritis (OA) is a chronic joint degenerative disease with no cure currently [1,2,3]
The results demonstrated that H2O2 induced robust cell viability reductions (Figure 1(b)) and cell death (Figure 1(c)), which were distinctly reversed by luteolin treatment
Treatment with luteolin alone failed to affect chondrocyte viability or cell death (Figures 1(d)–1(h)). These results suggested that luteolin treatment effectively protected chondrocytes from H2O2-elicited cell death and apoptosis
Summary
Osteoarthritis (OA) is a chronic joint degenerative disease with no cure currently [1,2,3]. The progressive chondrocyte apoptosis and extracellular matrix (ECM) degradation are the major pathogenic features of OA. Accumulating evidence has revealed that some oxidative stimuli will induce chondrocytes to generate reactive oxygen species (ROS) and inflammatory cytokines [4]. Inflammatory mediators, such as IL-1β and TNF-α, could damage the imbalance of cartilage homeostasis and activate inflammation response, resulting in chondrocyte apoptosis. As a major type of ROS, hydrogen peroxide (H2O2) induces mitochondrial damage, lipid peroxidation, and DNA damage, leading to ECM degradation and chondrocyte apoptosis [5]. Research on the discovery of novel and effective antioxidants to protect chondrocytes from oxidative injury has received increasing attention regarding OA treatment
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