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Amelioration of lipopolysaccharide (LPS)-induced inflammation via MAPK/NF-κB pathway in THP-1 macrophages and polystyrene microplastics (MPS)-induced inflammation, intestinal injury and dysbacteriosis in mice by a tropical coconut water-based postbiotic
Summary
Researchers tested whether a coconut water-based postbiotic could reduce inflammation caused by microplastics in both cell cultures and mice. The postbiotic suppressed inflammatory signaling pathways (NF-kB and MAPK) in immune cells and protected mice from microplastic-induced intestinal injury and gut microbial imbalance. The study suggests that fermented coconut water postbiotics may help mitigate some of the inflammatory and gut health effects associated with microplastic exposure.
Increasing accumulation of microplastics (MPS) in the human body poses potential health risks, such as chronic inflammation and intestinal injury and dysbacteriosis. Treatment to mitigate MPS’s injuries are urgent. This study aimed to investigate the effects of tender coconut water-based postbiotics (POS) on amelioration of lipopolysaccharide (LPS)-stimulated inflammation in THP-1 macrophages and MPS-induced physiological damage in mice. Firstly, the anti-inflammatory activity in vitro was evaluated by measuring the mRNA and protein expression of cytokines and mediators via qPCR, western blotting and ELISA. The metabolites profile was characterized by non-targeted metabolomics. MPS-exposure mice was utilized to verify the effects of POS on protecting from inflammation, intestinal injury and dysbacteriosis via ELISA, fluorescence histopathology, metagenomics, as well as short chain fatty acids (SCFAs) contents. Both POS and unfermented coconut water (CW) showed inhibition on Nuclear Factor-kappa B (NF-κB) and Mitogen-Activated Protein Kinase (MAPK) activation, while POS had a greater inhibitory effect. POS showed higher anti-inflammatory activity by significantly regulating mediators and cytokines’ gene transcription (Nrf2, HO-1, TNF-α, IL-6, IL1β, and IL-10), and secretion (IL-1β). Non-targeted metabolomics analysis showed that POS and CW were significantly separated in diversity, revealing the characteristic metabolites of POS and differential metabolic pathways. Animal study results revealed that POS rather than CW attenuated MPS-induced damage in mice by significantly decreasing aspartate transaminase, alanine aminotransferase, and pro-inflammatory factors, increasing Claudin-1 and Occludin expression, goblet cell numbers, gut microbiota richness and abundances, and butyric acid contents. These results provided a potential use of POS in MPS-induced damage.
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