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In the review of previous clinical and experimental studies, we find that tissues after external stimulation secrete cytokines including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), of which TNF-α stimulates the activation of other inflammatory mediators (including NF-κB), resulting in the release of inflammatory genes, and then leading to the persistence and deterioration of inflammation (Liu, 2005
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