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Additionally, TST was reported to be able to regulate thioredoxin metabolism, via using TXN as a sulfur-acceptor substrate and acting as a TXN oxidase, verse vice, TXN2 also reduces propenylsulfur protein to restore TST activity in a dose- and time-dependent manner [[62], [63], [64], [65]]
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Given Substance P’s relationship to neurokinin receptors, the success of NK antagonist usage in these clinical trials points to possible effectiveness in other Substance P-associated conditions [68,69,70,71]
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