Background  Previous studies have shown that leptin can promote osteoarthritis (OA) development by promoting the regulation of chondrocyte catabolism. Mitophagy is a critical protective mechanism for homeostasis maintenance, and defective mitophagy may lead to chondrocytes death and further develop into OA.

  Objective  To explore the role of leptin in the regulation of chondrocytes’ mitophagy and its relationship with cartilage degeneration, and elucidate the regulatory role of leptin in osteoarthritis (OA).

  Methods  Chondrocytes were isolated and cultured in vitro for leptin intervention. OA chondrocytes were divided into blank control group, low concentration (10 ng/ml) leptin group and high concentration (100 ng/ml) leptin group. Polymerase chain reaction (PCR) and Western blot were performed to detect the mRNA and protein expression of autophagy related molecules (Parkin, LC3A and LC3B) and MMP13. JC-1 probe was used to observe the changes of mitochondrial potential.

  Results  Compared with the control group, the autophagy related molecule LC3B was significantly lower in the low concentration group and the high concentration group by PCR and Western blot after leptin intervention (P＜0.05). However, the expression of MMP13 was significantly higher in the high concentration group (P＜0.05). The ratio of red to green fluorescence decreased after treated by leptin, and both the high and low concentration group decreased significantly (P＜0.05).

  Conclusion  Leptin may decrease mitochondrial membrane potential, inhibit mitophagy and promote cell catabolism, and therefore promote the progress of OA.