Resveratrol attenuated oxidative stress and inflammatory and mitochondrial dysfunction induced by acute ammonia exposure in gibel carp (Carassius gibelio)

Abstract

Ammonia is recognized as an environmental stressor for fish. As resveratrol (RES) has anti-inflammatory and antioxidant properties, we hypothesized that RES could attenuate the response to ammonia exposure in gibel carp. Therefore, gibel carp were fed a diet containing RES for eight weeks, followed by acute ammonia stimulation. Stress induced by acute ammonia exposure could be ameliorated by RES, manifested by down-regulated plasma glucose, and up-regulated C3 and IgM levels. Furthermore, decreased AST and LDH; enhanced T-AOC, SOD, and GPx in the liver; and reduced damage to gill and liver tissues indicated that RES attenuated oxidative and tissue damage induced by ammonia exposure. Moreover, RES activated the Nrf2/HO-1 pathway and up-regulated the expression of several antioxidant genes. RES enhanced anti-inflammatory activity as reflected by activation of the NF-κB pathway, down-regulated the expression of pro-inflammatory cytokines (nfκb, tnf-α, and il-1β), and up-regulated the expression of anti-inflammatory cytokines (il-4 and il-10). In terms of mitochondrial function, RES up-regulated protein levels of p-AMPK, SIRT1, and PGC-1α; inhibited mitochondrial fission; promoted mitochondrial fusion and biogenesis-related gene expression. Overall, the results suggest that RES mediated the Nrf2/HO-1, NF-κB, and AMPK/SIRT1/PGC-1α pathways to attenuate oxidative stress, inflammation, and mitochondrial dysfunction induced by ammonia in gibel carp.

Keywords: Ammonia; Inflammation; Mitochondrial dysfunction; Oxidative stress; Resveratrol.