10.1097/SHK.0b013e31826e47e8 Shock
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The proposed therapeutic mechanism involves the down-regulation of c-Jun-N-terminal kinase (JNK) by inducing Gadd45-beta activity, which ultimately disrupts a mechanism of mitochondrial damage.74 One investigative group in South Korea has reported on the use of sulforaphane (SFN) as a potential protector against oxidant-induced tissue injury.75 SFN is a dietary isothiocynanate synthesized from a precursor found in vegetables such as cauliflower, broccoli, kale, cabbage, collards and Brussels sprouts as well as other genera, such as the radish.75 SFN has been previously shown to have protective effects against oxidative stress-damaged tissues, such as the brain, heart, pancreas and kidney.75 In primary hepatocytes, cells pre-treated with SFN were shown to be protected against APAP-induced liver injuries via antioxidant actions by blocking generation of reactive oxygen species, depletion of GSH and peroxidation of lipids.75 Another group in China has suggested an association between adequate hepatocellular serotonin levels in murine models and protection against hepatocyte inflammation, oxidative stress, GSH depletion, peroxynitrite formation, elevated hepatocyte proliferation and reduction in several enzymes described in the process of hepatocyte necrosis.76 Human hepatocyte models are a next logical step, and thus more investigations need to be carried out before either serotonin or SFN can be realistically considered on the therapeutic level

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