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During an experimental study, when NFR-2 was activated in Treg, the inflammatory action was decreased due to the rise in Treg cellular levels [41] and, in another experimental method, it was proven that the anti-inflammatory mechanism is also found regardless of the presence of Treg [16] With synthetic antioxidants, NRF-2 can be activated in T cells determined by the rise in the antioxidant response elements mediated by NRF-2, as well as the suppression of IFN- and the concomitant production of the cytokines of Th2 lymphocytes, such as IL-4, IL-5, and IL-13

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However, with BPC 157 therapy, both skin and esophageal defect may be closed without mortality (Cesarec et al., 2013)

& Uceyler, N