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Similarly, exenatide ameliorated the inflammatory response in human RA FLSs by decreasing the oxidative stress capacity of FLSs and down-regulating the expression of IL-1 and IL-6, while suppressing the initiation of p38/MAPK and NF-B signal transduction pathways [240]

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Since then, there have been a handful of additional reports of a possible association (12-14)

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