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N-alkyl-hydroxybenzoyl anilide hydroxamate (AHBAH) prevents osteoarthritis in rats through promotion of chondrocyte proliferation

Osteoarthritis caused by the decomposition of bones at joints is associated with movement loss and severe pain. In the present study mechanism and role of N-alkyl-hydroxybenzoyl anilide hydroxamate (AHBAH) in the prevention of osteoarthritis in rats was investigated. Osteoarthritis was established by giving monosodium iodoacetate (MIA; 5 mg/kg) injections to rats through an intra-articular route. Rats were separated into sham, model and AHBAH (at 0.5, 1.0 and 2.0 mg/kg doses). Single doses of AHBAH were given to rats 1 day prior to MIA-injection intraperitoneally. Chondrocyte proliferation showed a significant (p < 0.05) enhancement on treatment with AHBAH in 0.5-10 μM concentration range. The G0/G1 phase proportion of chondrocytes showed a decrease while as percentage in S and G2/M phases increased on treatment with AHBAH. In AHBAH-treated chondrocytes expression of cyclin D1, cyclin-dependent kinase (CDK)-4, and CDK6 were promoted whereas inflammatory cytokine levels were suppressed. The inhibitor of nuclear factor kappa B (IκB)-α and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 expression in AHBAH-treated OA rats was significantly inhibited compared to the model group. Thus, AHBAH promotes chondrocyte proliferation by increasing G1/S phase transition. Additionally, AHBAH exhibited an inhibitory effect on inflammatory cytokine secretion in osteoarthritis rats. Therefore, AHBAH can be of therapeutic importance for osteoarthritis treatment and may be studied further.