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On the basis of the findings by Narita et al. [3] demonstrating that RJ stimulates bone formation, we used the osteoblastic cell line KS483 followed by the Alizarin Red-S staining as a model system to study the effect of FAs on the mineralization process [20], which is known to be an estrogen induced effect.
Since the contribution of synovial fibroblasts to inflammation and joint destruction is crucial, the potential activating effect of Fas on mouse fibroblast cell line NIH3T3 was investigated.
Despite few studies describing a caspase-dependent inhibitory effect of Fas on NF- κB, it is usually accepted that Fas induces NF- κB.
Since cytokines such as TNF-α and IL-6 are critical mediators of inflammation, we investigated the effect of Fas on the expression of proinflammatory cytokines in joints.
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Accelerated aging (exposure to continuous sodium hydroxide at 38 °C and sodium chloride solutions at room temperature) and tests of transport properties (salt ponding, rapid chloride permeability and sorptivity tests) are used to study the effect of FA on the durability of the ECC.
This study estimates the effect of FA on outcomes on FA recipients.
These effects all suggest a possible effect of FA on protein synthesis and turnover.
Last, some studies report the effect of FA on the total number of PTB.
None of these targets appears to explain the effect of FA on caspase-3.
Unexpectedly, we identified a striking effect of FA on genes involved in developmental processes, cell adhesion and G protein signaling.
The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth.
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