The protective effect of Ganoderma atrum polysaccharide on intestinal barrier function damage induced by acrylamide in mice through TLR4/MyD88/NF-κB based on the iTRAQ analysis

The potential mechanism for the protective effect of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrylamide (AA) induced intestinal damage in mice was explored. Results showed that PSG-1 pretreatment prevented AA-induced injury by decreasing intestinal permeability and serum D-lactate acid (D-Lac) levels and increasing the number of small intestinal goblet cells and IgA secreting cells. In addition, PSG-1 pretreatment effectively reduced malondialdehyde (MDA) level and raised superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) activities in the intestine. Furthermore, PSG-1 administration decreased the levels of pro-inflammatory factors including IL-1 beta, TNF-alpha, and IL-6, while the anti-inflammatory factor IL-10 was elevated. Meanwhile, PSG-1 could increase the performance of tight junction (TJ) proteins such as Occludin, Claudin-1 and ZO-1. Moreover, according to the isobaric tag for relative and absolute quantitation (iTRAQ) and Western blot results, PSG-1 could reduce AA-induced intestinal injury through TLR4/MyD88/NF-kappa B signaling pathway. Overall, the present study suggested that PSG-1 protected intestinal permeability and barrier function in mice via reducing inflammation and oxidative stress, and effectively prevented AA-induced intestinal injury in mice.

Automated summary

The protective effects of Ganoderma atrum polysaccharide (PSG-1) on acrylamide-induced intestinal damage in mice were investigated. PSG-1 pretreatment effectively prevented injury by reducing intestinal permeability and serum D-lactate acid levels, increasing goblet and IgA secreting cells, decreasing oxidative stress, inflammation, and enhancing tight junction proteins. Furthermore, PSG-1 was found to exert its protective effects through the TLR4/MyD88/NF-kappa B signaling pathway.