Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway

Sodium acetate/sodium butyrate alleviates lipopolysaccharide-induced diarrhea in mice via regulating the gut microbiota, inflammatory cytokines, antioxidant levels, and NLRP3/Caspase-1 signaling

“…The current results were in line with a study on inflammatory bowel disease in humans with the downregulation of Occludin (Chen et al, 2015). The expression of Claudin in group L was significantly lower, which is in line with previous results (He et al, 2022); however, with the treatment of sodium acetate/sodium butyrate, the expression of Claudin upregulated significantly. The plaque protein ZO1 is an adaptor connecting trans-membrane protein with the peri-junctional actomyosin ring (Ulluwishewa et al, 2011).…”

“…In the present study, mice were supplemented with sodium acetate/sodium butyrate before inducing diarrhea by utilizing LPS. Serve damage to intestines particularly jejunum, ileum, cecum, and colon was examined ( Figure 1B ), which was in accordance with previous results ( He et al, 2022 ). An obvious decrease in villus height, increase in crypt depth, and lowered villus height to crypt depth ratio were uncovered in group C, while interestingly, sodium acetate/sodium butyrate supplementation could significantly increase the villus height, decrease the crypt depth, and increase the villus height to crypt depth ratio in both jejunum and ileum, especially in groups B and A ( Figures 1C,D ).…”

“…The plaque protein ZO1 is an adaptor connecting trans-membrane protein with the peri-junctional actomyosin ring ( Ulluwishewa et al, 2011 ). Like previous results found lower expressions of ZO-1 ( Cao et al, 2022 ; He et al, 2022 ), the expression of ZO-1 in group L was significantly higher than in group C, while expression levels of ZO-1 decreased in sodium acetate/sodium butyrate-treated groups. The current findings suggested that acetate/sodium butyrate could improve intestinal barrier function by modulating tight junction gene expressions.…”

“…The widely known lipopolysaccharide is an important membrane component of gram-negative bacteria, causing the inflammatory reaction, oxidative damage, and gut dysbiosis in hosts ( Xu et al, 2021 ). Previous studies found that ROS were an important second messenger of the atypical domain (NOD)-like receptor containing pyrin domain 3 inflammasomes, and Caspase-1 was activated by NLRP3 and then cause inflammation reaction ( Dashdorj et al, 2013 ; Sho and Xu, 2019 ; He et al, 2022 ). Hence, we conducted this study to explore the alleviation effect and potential mechanism of sodium acetate/sodium butyrate supplementation on LPS-induced diarrhea in mice via NLRP3/Caspase-1 signaling.…”

Di-(2-Ethylhexyl) Phthalate and Microplastics Induced Neuronal Apoptosis through the PI3K/AKT Pathway and Mitochondrial Dysfunction

“…Benefiting from its small size, MPs can easily break through barriers and cause injury to various tissues of fish, rodents, and mammals. − MPs passe through the food chain to threaten biological health . Furthermore, reports have shown that MPs can cause inflammation and necroptosis in the liver, spleen, kidneys, and other organs. − Based on the widespread presence of DEHP and MPs in nature, there is a possibility of them being present in the human body. However, there are still gaps in the study of the destructive effects and underlying mechanisms of action of DEHP and MPs on neurons in the cerebrum, as well as the neurotoxicity of the cerebrum caused by the combination of DEHP and MPs.…”