Study Title:

Leptin protects rat articular chondrocytes from cytotoxicity induced by TNF-α in the presence of cyclohexamide

Study Abstract:

OBJECTIVE:

Although leptin appears to be an important local and systemic factor influencing cartilage homeostasis, the role of leptin in chondrocyte death is largely unknown. TNF-α is a pro-inflammatory cytokine that plays a central role in the pathogenesis of articular diseases. This study examines whether leptin modulates TNF-α-induced articular chondrocyte death.
METHODS:

Primary rat articular chondrocytes were isolated from knee joint cartilage slices. To induce cell death, the chondrocytes were treated with TNF-α. To examine whether leptin modulates the extent of TNF-α-mediated chondrocyte death, the cells were pretreated with leptin for 3 h before TNF-α treatment followed by viability analysis. To examine the mechanism by which leptin modulates the extent of TNF-α-mediated chondrocyte death, we utilized mitochondrial membrane potential measurements, flow cytometry, nuclear morphology observation, coimmunoprecipitation, western blot analysis and confocal microscopy.
RESULTS:

We demonstrated that leptin suppresses TNF-α induced chondrocyte death. We further found that apoptosis partially contributes to TNF-α induced chondrocyte death while necroptosis primarily contributes to TNF-α induced chondrocyte death. In addition, we observed that leptin exerts anti-TNF-α toxicity via JNK in rat articular chondrocytes.
CONCLUSION:

Based on our findings, we suggest that the leptin present in the articular joint fluid protects articular chondrocytes against cumulative mechanical load and detrimental stresses throughout a lifetime, delaying the onset of degenerative changes in chondrocytes. We can further hypothesize that leptin protects articular chondrocytes against destructive stimuli even in the joints of OA patients.

Study Information:

 Leptin protects rat articular chondrocytes from cytotoxicity induced by TNF-α in the presence of cyclohexamide Osteoarthritis Cartilage. 2015 June 

Full Study:

http://www.ncbi.nlm.nih.gov/pubmed/26074364

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