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There is a growing amount of research that highlights the significant connection between the development of colitis and both metabolic imbalance and the inflammatory response. Tagatose, an inherent sweetening agent and alternative to sugar, plays a crucial role in the biosynthesis of several chemicals and metabolic pathways in living organisms. However, the specific biochemical mechanism via which tagatose hinders colitis is still not understood. According to recent study, tagatose plays a crucial role in safeguarding the integrity of tight junctions inside the intestinal mucosal barrier. Furthermore, it is crucial to acknowledge the presence of a correlation between the severity of inflammatory bowel disease (IBD) and the occurrence of colorectal cancer (CRC), chemically-induced colitis in rodents, and reduced blood levels of tagatose. The treatment of tagatose resulted in a decrease in intestinal mucosal injury in mice with colitis, regardless of whether it was caused by dextran sodium sulfate (DSS) or spontaneous colitis in IL-10-/- mice and C3H/HeJBir mice. The introduction of tagatose in a colitis model triggers a cascade of events, wherein it hinders the expulsion of cathepsin B and enhances lysosomal cohesiveness. The aforementioned method successfully inhibits the activity of myosin light chain kinase (MLCK) in the context of intestinal epithelial damage, hence impeding the deterioration of tight junction integrity and the initiation of mitochondrial dysfunction. In summary, the outcomes of the study have provided empirical evidence that substantiates the beneficial effects of tagatose in mitigating the progression of colitis. The ability to prevent the disruption of the intestinal barrier is responsible for this achievement. Hence, tagatose has promise as a therapeutic adjunct for the management of colitis.

Rotifer Brachionus rotundiformis is the first live food for larval fish that can generally be plagued by ammonia (AC) in intensive culture systems. Ammonia accumulates enough to cause rotifer death. L-carnitine (LC) as a supplement of a vitamin-like nutrient can ameliorate rotifer growth performance and reproduction. The present study investigated the effects of LC on growth performance, antioxidant enzymatic activity, bacterial numbers and eradication of AC toxicity in rotifer. During a 7-day culture experiment added different concentration LC, Acute toxicity tests of AC and a batch culture experiment treated with LC and AC were performed. The results indicated that suitable LC concentration (1−100 mgL−1) treatment promoted significantly the rotifer population growth, while the AC was opposite and the AC median lethal concentration (LC50)-24 h was 12.24 mg L-1. Batch culture results showed that, under AC stress, LC significantly increased the rotifer population density and egg rate, and reduced rotifer malondialdehyde (MDA) level, increased rotifer Superoxide dismutase (SOD), Catalase (CAT), glutathione peroxidase (GPx) and total antioxidant capacity (T-AOC) activities. For the bacterial numbers, all treatments presented an increasing trend during the culture period, and there was a significant correlation with the rotifer population density especially in the group LC + AC. Overall, our results indicate that the rotifer growth can be inhibited by the AC, and under AC stress, LC can also improve the population growth, anti-stress ability of rotifer and the bacterial numbers in the medium. The amelioration of rotifer-growth may be linked to the anti-stress ability and the bacterial numbers.

High nutritive microalgae is a key factor that affecting the live feeds nutritional value and subsequently fish fry quality. We evaluated the effect of l-carnitine supplementation level on the population growth, photosynthetic pigment biosynthesis, and antioxidant capability of the pigment-protein complexes in the marine Chlorella sp. Five different l-carnitine levels (0, 5, 50, 100, and 200 mg L−1) were supplemented in the microalgae media for 10 days. The results demonstrated that l-carnitine increased the population density and specific growth rate in LC 5 (P < 0.05). While the β-carotene and iron contents were elevated in LC 5 and LC 50 (P < 0.05). Apart from, chlorophyll a, chlorophyll b, and magnesium contents were higher in the LC 5 (P < 0.05). While LC 5 had higher metal chelation in pigment-protein complexes (P < 0.05). Meanwhile, psy and chld gene expressions were up-regulated in the LC 5 and LC 50 (P < 0.05). Taken together, LC 5 and LC 50 could improve the population growth, pigment synthesis, antioxidant capacity and up-regulate the relative expression levels of photosynthetic pigment synthesis genes in marine Chlorella sp. Therefore, l-carnitine has comprehensive effects on algae production.

Endothelial-to-mesenchymal transition (EndMT) is closely related to the pathogenesis of various diseases, including cardiac fibrosis. Transforming growth factor (TGF)-β1 strongly induces EndMT, and sirtuin 1 (SIRT1) may play vital roles in TGF-β/Smad pathway inhibition. This study aimed to determine whether SIRT1 activation inhibits EndMT, thereby attenuating cardiac fibrosis. Cardiac fibrosis was induced in C57BL/6 mice by subcutaneously injecting isoproterenol. SIRT1 was activated and then suppressed by intraperitoneally injecting resveratrol (RSV) and EX527, respectively. EndMT was induced by adding TGF-β1 to H5V cells and measured by immunofluorescence and western blot. The role of SIRT1 in EndMT was determined by lentivirus-mediated overexpression of SIRT1. Interactions between SIRT1 and Smad2/3 in the TGF-β/Smad2/3 pathway were examined by immunoprecipitation. SIRT1 activation upregulated CD31 and vascular endothelial-cadherin, and downregulated α-smooth muscle actin, fibroblast-specific protein 1, and vimentin. SIRT1 upregulated and EX527 inhibited TGF-β receptor 1 (TGF-βR1) and P-Smad2/3 expression, respectively. SIRT1 activation and overexpression by RSV/SRT2104 and lentivirus transfection, respectively, reduced TGF-β1-induced EndMT. SIRT1 and Smad2/3 interaction was shown by immunoprecipitation in vivo and in vitro. TGF-βR1 and P-Smad2/3 expression was downregulated and Smad2/3 nuclear translocation was inhibited. In conclusion, SIRT1 activated by RSV attenuated isoproterenol-induced cardiac fibrosis by regulating EndMT via the TGF-β/Smad2/3 pathway.