The experiment was aimed at examining the influence of adding emodin to feeds on the growth performance, liver immunity, and resistance against Aeromonas veronii infection among juvenile largemouth basses and other potential mechanisms. A total of 540 fish (45 ± 0.3 g) were randomly divided into 6 diets, including EM-0, EM-250, EM-500, EM-1000, EM-2000, and EM-4000 diets, in which 0, 250, 500, 1000, 2000, and 4000 mg kg⁻¹ emodin was added. Following a 60-day feeding test, it demonstrated that the feed conversion ratio (FCR) of juveniles within the EM-500 and EM-1000 groups remarkably exceeded that of the EM-0 group. Subsequently, unlike those in EM-0 group, the fish in the EM-1000 group showed heightened hepatocyte count, induced hepatic lipolysis-associated expression of peroxisome proliferators-activated receptor α (PPARα) and acyl-coenzyme an oxidase (ACO), and reduced the hepatic triglyceride (TG) levels. Additionally, EM-1000 could up-regulate the expressions of nuclear factor erythroid 2-associated factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in livers compared with controls and boost antioxidant enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), along with a lower content of reactive oxygen species (ROS) and malondialdehyde (MDA). Meanwhile, the EM-1000 group increased anti-inflammatory cytokines of interleukin-10 (IL-10) while suppressing the interleukin-8 (IL-8) expression of pro-inflammatory cytokines in livers by contrast to controls. In the end, juvenile largemouth bass in the EM-1000 group showed a comparatively highest survival rate, whereas fish in the EM-2000 and EM-4000 groups exhibited a little higher mortality than that of the EM-0 group. To sum up, our study exposed that supplementing emodin with 1000 mg kg⁻¹ in diet could enhance the hepatic antioxidant status and unspecific immunity to reinforce the protective effect on disease resistance, resulting in improving the growth performance in juvenile largemouth bass.

The effects of starvation and refeeding on the gut condition of juvenile largemouth bass (Micropterus salmoides) remain unclear. Therefore, our research aimed to explore these effects. Amylase and lipase activities were remarkably decreased in the starvation (ST) group, yet prominently increased in the refeeding (RE) group (p < 0.05). In addition to the malondialdehyde (MDA) level, catalase (CAT) and superoxide dismutase (SOD) activities were significantly upregulated in the ST group (p < 0.05) in marked contrast to those in the controls; however, the RE group showed no substantial variations in CAT and SOD activities or the MDA level (p > 0.05). During starvation, the expression of Nrf2-Keap1 pathway-associated genes was significantly upregulated (p < 0.05). The comparative levels of TNF-α, IL-1β, and IL-15 were highly increased, with the levels of TGF-β1 and IL-10 apparently downregulated in the ST group; in contrast, these levels were restored to their original values in the RE group (p < 0.05). In contrast to the controls, the ST group showed significantly lower height and width of the villi, muscle thickness, and crypt depth and a higher goblet cell number; however, these values were recovered to some extent in the RE group (p < 0.05). The dominant bacterial phyla in the intestines of both groups were Proteobacteria, Firmicutes, Bacteroidetes, Acidobacteria, and Actinobacteria, with marked inter-group differences in the genera Serratia and Lactobacillus. Metabolomics analysis showed that amino acid metabolism is disrupted during starvation and is restored after refeeding. In summary, this study expands our comprehension of the interaction between oxidative stress and antioxidant defenses among juvenile largemouth bass subjected to starvation and refeeding.