Optimal DL-Methionyl-DL-Methionine Supplementation Improved Intestinal Physical Barrier Function by Changing Antioxidant Capacity, Apoptosis and Tight Junction Proteins in the Intestine of Juvenile Grass Carp (Ctenopharyngodon idella)

Abstract

The present study was a part of a larger research project that aimed to investigate the effects of Met-Met supplementation on fish growth and intestinal health. This study mainly focused on the relationship between dietary Met-Met and intestinal physical barrier function in fish. Seven iso-nitrogenous diets supplemented with 2.50 g/kg DL-methionine (DL-Met) and six graded levels of Met-Met (0.00, 0.79, 1.44, 1.84, 2.22, and 2.85 g/kg) were used to feed juvenile grass carp for 10 weeks, after which a 14-day Aeromonas hydrophila challenge test was performed. The results indicated that optimum levels of Met-Met decreased intestinal oxidative damage, probably by increasing total antioxidant capacity, and the activity and gene expression levels of several antioxidant enzymes, which were closely related to the changed Nrf2/Keap1 signaling. Meanwhile, optimum levels of Met-Met decreased intestinal apoptosis and improved the intestinal tight junction, as evident by the downregulated mRNA levels of initiator and executioner caspases; the pro-apoptotic-related proteins FasL, Apaf-1, and Bax; and upregulated mRNA levels of the anti-apoptotic proteins Bcl-2, Mcl-1b, and IAP and the TJ proteins claudins, occludin, and ZOs. Furthermore, the positive effects of Met-Met on improving intestinal physical barrier function were superior to those of DL-Met in fish. These findings showed that optimal Met-Met supplementation improved intestinal physical barrier function, probably by changing antioxidant capacity, apoptosis, and tight junction proteins in fish.

Repositioning of the Antihyperlipidemic Drug Fenofibrate for the Management of Aeromonas Infections

“…Because the physiological role of BAX is to maintain cell and tissue homeostasis, any dysregulation of BAX results in abnormal cell death [ 56 ]. It has been previously reported that some species of Aeromonas are able to induce the overexpression of proinflammatory cytokines, chemokines, and genes related to apoptosis [ 33 , 57 ], as we have observed with the strains studied in this work. In some cases, this overexpression is maintained during infection and is partially responsible for cytokine storm, a systemic inflammatory response that increases the infection severity [ 58 ].…”

Fermented Astragalus membranaceus could promote the liver and intestinal health of juvenile tiger grouper (Epinephelus fuscoguttatus)

“…The reason may be that short-chain fatty acids (Qiao, 2020) or other prebiotics are produced during the fermentation process of AM, which promotes the growth of beneficial bacteria, inhibits harmful bacteria, improves the homeostasis of intestinal environment, and thus facilitates the development of intestinal mucosa (Cheng et al, 2021). The improvement of intestinal morphology enhances the intestinal barrier function, improves the immune and pathogenic microbial defense ability, and may reduce intestinal cell apoptosis (Wu et al, 2022a), and ultimately has a positive impact on the body's nutrient utilization and growth (Yang et al, 2022). The intestinal microbiota of fish is essential for maintaining the health of aquatic animals (Wang et al, 2021b).…”

Protective Effect of Alpinia oxyphylla Fructus Polysaccharides Extracted with Different Solvents on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice

“…Te pathogenesis of UC is closely linked to the intestinal barrier, intestinal fora, and immunity. Te intestinal barrier composed of intestinal epithelial cells and tight junctions (TJ) is the frst defensive site for the invasion of toxoid and pathogenic bacteria, and if the intestinal epithelial cells and TJ are disrupted, excessive oxidative stress and infammatory reactions can be induced, leading to the deterioration of UC [6,7]. Research has found that Agaricus blazei Murrill polysaccharides attenuate dextran sulfate sodium (DSS)induced colitis and protect the colon barrier from damage by decreasing MDA, TNF-α, IL-1β, and IL-6 levels and elevating SOD and IL-10 levels [8].…”