Synovial interlukin-6 affects apoptosis induction via nuclear factor kappa-B and fractalkine pathway during adjuvant arthritis

Apoptosis disruptions play substantial roles in pathogenesis of arthritis and its symptoms. Cytokines and their intra-cellular signaling have pivotal roles in arthritis pathophysiology. The present study aimed to investigate the relation between synovial Interleukin- 6 (IL-6), Nuclear Factor Kappa- B (NF-ĸB) and Fractalkine (Fkn) in the changes of edema and apoptosis during Adjuvant-induced knee arthritis.

240 male Wistar rats were divided into different groups. Arthritis was evoked and the knee edema changes were evaluated by Vernier caliper. Synovial IL-6 was assayed by rat standard ELISA kit. Synovial NF-ĸB, Fkn, and markers of apoptosis were measured by western blot experiment.

The injection of Complete Freundchr('39')s Adjuvant (CFA) caused intense knee edema reduced by implementing Anti-IL-6, Anti-Fkn and Inh-NF-ĸB. The results indicated elevated levels of apoptotic markers during the acute phase, along with an increase in IL-6, NF-ĸB and Fkn. Although IL-6, NF-ĸB and Fkn levels elevation continued during chronic phase, the apoptosis markers decreased in this phase. The findings revealed that Anti-IL-6 treatment during different phases of study can change the synovial NF-ĸB and Fkn.

It seems that time-dependent variations in apoptotic markers level may be involved in pathogenesis of Adjuvant-induced knee arthritis. In conclusion, synovial IL-6 through NF-ĸB- Fkn pathway can play an important role in this process.
Keywords: Apoptosis, Adjuvant, Fractalkine, IL-6, Inflammation, NF-ĸB