Lipopolysaccharide (LPS) as a major component of Escherichia coli cell wall can cause inflammation and cell death. Dihydromyricetin (ampelopsin, DHM) is a natural flavonoid compound with anti-inflammatory, anti-oxidant and anti-bacterial effects. The preventive effects of DHM against ileum injury remain unclear. Here, we explored the protective role of DHM against LPS-induced ileum injury in chickens. In this study, DHM significantly attenuated LPS-induced alteration in diamine oxidase, malondialdehyde, reduced glutathione, glutathione peroxidase and superoxide dismutase levels in chicken plasma and ileum. Histology evaluation showed that the structure of blood vessels in ileum was seriously fragmented and presence of necrotic tissue in the lumen in the LPS group. Scanning electron microscopic observation revealed that the surface of the villi was rough and uneven, the structure was chaotic, and the normal finger shape was lost in the LPS group. In contrast, 0.05% and 0.1% DHM treatment partially alleviated the abnormal morphology. Additionally, DHM maintained the barrier function by restoring the protein expression of occludin, claudin-1 and zonula occludens protein-1. DHM inhibited apoptosis through the reduction of the expression of bax and caspase-3 and restored the expression of bcl-2. Importantly, DHM could reduce ileum NLR family pyrin domain-containing 3 (NLRP3), caspase-1, interleukin (IL)-1β and IL-18 expression to protect tissues from pyroptosis and inhibited toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signalling pathway. In summary, DHM attenuated the ileum mucosal damage, oxidative stress and apoptosis, maintained barrier function, inhibited NLRP3 inflammasome and TLR4/NF-κB signalling pathway activation triggered by Escherichia coli LPS.

These results suggested that S. nigrum has hepatoprotective effects against ethanol-induced injury both in vitro and in vivo, and can protect the integrity of hepatocytes and thus reduce the release of liver GSTA1, which contributes to improved liver detoxification.

Bacterial biofilms have been demonstrated to be closely related to clinical infections and contribute to drug resistance. Berberine, which is the main component of Coptis chinensis, has been reported to have efficient antibacterial activity. This study aimed to investigate the potential effect of a combination of berberine with ciprofloxacin (CIP) to inhibit Salmonella biofilm formation and its effect on expressions of related genes (rpoE, luxS, and ompR). The fractional inhibitory concentration (FIC) index of the combination of berberine with CIP is 0.75 showing a synergistic antibacterial effect. The biofilm's adhesion rate and growth curve showed that the multi-resistant Salmonella strain had the potential to form a biofilm relative to that of strain CVCC528, and the antibiofilm effects were in a dose-dependent manner. Biofilm microstructures were rarely observed at 1/2 × MIC/FIC concentrations (MIC, minimal inhibition concentration), and the combination had a stronger antibiofilm effect than each of the antimicrobial agents used alone at 1/4 × FIC concentration. LuxS, rpoE, and ompR mRNA expressions were significantly repressed (p < 0.01) at 1/2 × MIC/FIC concentrations, and the berberine and CIP combination repressed mRNA expressions more strongly at the 1/4 × FIC concentration. The results indicate that the combination of berberine and CIP has a synergistic effect and is effective in inhibiting Salmonella biofilm formation via repression of luxS, rpoE, and ompR mRNA expressions.

The results of our investigation suggested that FS ethanol extracts possess significant protective effects against hepatotoxicity induced by acetaminophen both in vitro and in vivo. In addition, GSTA1 could be used as an indicator assessing the extents of hepatic injury, which is more sensitive than transaminases.

Abstract. In the present study, three models of acute liver injury in mice were induced via the administration of CCl 4 (35 mg/kg, 24 h), acetyl-para-aminophenol (APAP; 200 mg/kg, 12 h) and ethanol (14 ml/kg, 8 h) to study the effect of glutathione S-transferase A1 (GSTA1) on acute liver injury. The serum levels of alanine transaminase, aspartate transaminase and liver homogenate indicators (superoxide dismutase, glutathione and glutathione peroxidase) were significantly lower in model groups compared with the control group (P<0.01), whereas the liver homogenate indicator malondialdehyde was significantly increased (P<0.01). The expression of GSTA1 in liver was significantly decreased in the model groups compared with the control group (P<0.01). GSTA1 protein content was 3.8, 1.3 and 2.6 times lower in the CCl 4, APAP and ethanol model groups, respectively. Furthermore, GSTA1 mRNA expression levels decreased by 4.9, 2.1 and 3.7 times in the CCl 4, APAP and ethanol model groups, respectively. Among the three models, the injury induced by CCl 4 was the most marked, followed by ethanol and finally APAP. These results suggest that GSTA1 may be released by the liver and serve as an antioxidant in the prevention of liver damage. IntroductionLiver disease poses a serious threat to human health and food safety, as consumption of animals with liver disease may be detrimental to health (1). Acute liver injury is the common pathway and initiating factor of many liver diseases, such as acute liver failure (2). Three models of liver injury are typically used in research as they are representational and reflect the situation of hepatotoxicity comprehensively and intuitively (3). CCl 4 is a classical hepatotoxicant, which is able to induce reactive oxygen formation and deplete glutathione (GSH) (4). Acetyl-para-aminophenol (APAP) hepatotoxicity is induced by the electrophile N-acetyl-p-benzoquinoneimine (NAPQI), which is able to induce mitochondrial dysfunction and oxidative stress, leading to liver damage (5). The major etiological factors of hepatotoxicity in ethanol-induced hepatic injury are oxidative stress and inflammatory responses (6). Due to the complexity of liver function and the diversity of liver damage factors, experimental animal models are not able to accurately and fully reflect the nature of liver injury (7). Furthermore, existing animal models have various limitations such as non-standardized methods, lack of reproducibility and non-unified methods (8).Glutathione S-transferases (GSTs) are enzymes that are able to protect cells from damage caused by reactive oxygen species (9). GSTA (α class GST) serves an important cytoprotective role in detoxifying reactive electrophiles and products of lipid peroxidation (10). GSTs including GSTA have previously been identified as inhibitors of stress-activated kinase activity, most notably c-Jun N-terminal kinase (11). This suggests that altered GST expression may be an important factor in modulating the cellular transition between proliferation, differentiation, and apo...