Chlorogenic acid, a natural phenolic acid present in fruits and plants, provides beneficial effects for human health. The objectives of this study were to investigate whether chlorogenic acid (CHA) could improve the intestinal barrier integrity for weaned rats with lipopolysaccharide (LPS) challenge. Thirty-two weaned male Sprague Dawley rats (21±1 d of age; 62.26±2.73 g) were selected and randomly allotted to four treatments, including weaned rat control, LPS-challenged and chlorogenic acid (CHA) supplemented group (orally 20 mg/kg and 50 mg/kg body). Dietary supplementation with CHA decreased (P<0.05) the concentrations of urea and albumin in the serum, compared to the LPS-challenged group. The levels of IFN-γ and TNF-α were lower (P<0.05) in the jejunal and colon of weaned rats receiving CHA supplementation, in comparison with the control group. CHA supplementation increased (P<0.05) villus height and the ratio of villus height to crypt depth in the jejunal and ileal mucosae under condictions of LPS challenge. CHA supplementation decreased (P<0.05) intestinal permeability, which was indicated by the ratio of lactulose to mannitol and serum DAO activity, when compared to weaned rats with LPS challenge. Immunohistochemical analysis of tight junction proteins revealed that ZO-1 and occludin protein abundances in the jejunum and colon were increased (P<0.05) by CHA supplementation. Additionally, results of immunoblot analysis revealed that the amount of occludin in the colon was also increased (P<0.05) in CHA-supplemented rats. In conclusion, CHA decreases intestinal permeability and increases intestinal expression of tight junction proteins in weaned rats challenged with LPS.

The intestinal epithelial layer forms a barrier through cell–cell tight junctions and breaking or even slightly disrupting this barrier can lead to serious pathological consequences, including infection and inflammation. Various amino acids have been shown to improve the intestinal tract, but the effect of tryptophan on the intestinal barrier has been controversial. Here, an in vitro Caco-2 cell model was built to investigate the protective and reparative effects of different concentrations of dietary L-Tryptophan (L-Trp) on lipopolysaccharide (LPS)-induced intestinal tight junction injury. Lower concentrations (40 μM) of dietary L-Trp protected and repaired the integrity and permeability injury of the intestinal tight junction induced by LPS, while high concentrations (80 μM) may not have a positive effect. LPS-induced injury led to increased (P < 0.05) mRNA expression of Nuclear factor-kappa B (NFκB) and Myosin light-chain kinase (MLCK), and decreased (P < 0.05) the mRNA expression of extracellular regulated protein kinase 1/2 (ERK1/2) and Mitogen-activated protein (MAP), and the treatment of dietary L-Trp alleviated those regulations in different concentrations, which suggests that dietary L-Trp may attenuate LPS-induced injury to tight junctions via inhibiting the NFκB-MLCK signaling pathway and activating the ERK1/2-MAP signaling pathway. And the mRNA and protein expressions of claudin-1, occludin and ZO-1 in LPS-induced injury were all down-regulated to varying degrees, and dietary L-Trp weakened the down-regulation of claudin-1 (P < 0.05) with no significant regulation of the protein expression of occludin and ZO-1 (P > 0.05).

Uridine (UR) is a pyrimidine nucleoside that plays an important role in regulating glucose and lipid metabolism. The aim of this study was to investigate the effect of UR on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet (HFD)-fed mice. ICR mice were, respectively, divided into 3 groups for 8 weeks, that is, control (CON, n = 12), high fat diet (HFD, n = 16), and HFD + UR groups (0.4 mg mL⁻¹ in drinking water, n = 16). UR supplementation significantly reduced the body weight and suppressed the accumulation of subcutaneous, epididymal, and mesenteric WAT in HFD-fed mice (P < 0.05). Meanwhile, UR also decreased the lipid droplet accumulation in the liver and liver organoids (P < 0.05). In addition, UR supplementation increased bacterial diversity and Bacteroidetes abundance, and decreased the Firmicutes-to-Bacteroidetes ratio in HFD-fed mice significantly (P < 0.05). UR promoted the growth of butyrate-producing bacteria of Odoribacter, unidentified-Ruminococcaceae, Intestinimonas, Ruminiclostridium, and unidentified-Lachnospiraceae. A close correlation between several specific bacterial phyla or genera and the levels of WAT weight, hepatic TC, or hepatic TG genera was revealed through Spearman's correlation analysis. These results demonstrated that UR supplementation could be beneficial by attenuating HFD-induced obesity and nonalcoholic fatty liver disease.

Antimicrobial blue light (aBL) has attracted increasing interest for its antimicrobial properties. However, the underlying bactericidal mechanism has not yet been verified. One hypothesis is that aBL causes the excitation of intracellular chromophores; leading to the generation of reactive oxygen species (ROS) and the resultant oxidization of various biomolecules. Thus, monitoring the levels of redox-sensitive intracellular biomolecules such as coproporphyrins, as well as singlet oxygen and various ROS may help to uncover the physiological changes induced by aBL and aid in establishing the underlying mechanism of action. Furthermore, the identification of novel targets of ROS, such as fatty acids, is of potential significance from a therapeutic perspective. In this study, we sought to investigate the molecular impact of aBL treatment on methicillin-resistant Staphylococcus aureus (MRSA). The results showed that aBL (5–80 J/cm²) exhibited a bactericidal effect on MRSA, and almost no bacteria survived when 80 J/cm² had been delivered. Further studies revealed that the concentrations of certain intracellular molecules varied in response to aBL irradiation. Coproporphyrin levels were found to decrease gradually, while ROS levels increased rapidly. Moreover, imaging revealed the emergence and increase of singlet oxygen molecules. Concomitantly, the lipid peroxidation product malondialdehyde (MDA) increased in abundance and intracellular K⁺ leakage was observed, indicating permeability of the cell membrane. Atomic force microscopy showed that the cell surface exhibited a coarse appearance. Finally, fatty acid profiles at different illumination levels were monitored by GC-MS. The relative amounts of three unsaturated fatty acids (C_16:1, C_20:1, and C_20:4) were decreased in response to aBL irradiation, which likely played a key role in the aforementioned membrane injuries. Collectively, these data suggest that the cell membrane is a major target of ROS during aBL irradiation, causing alterations to membrane lipid profiles, and in particular to the unsaturated fatty acid component.