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Polysaccharides are one of the main active substances in Ganoderma atrum (G. atrum). The purpose of this study was to explore the protective effect of a G. atrum polysaccharide (PSG-1) on DSS-induced colitis and the underlying mechanism. The results showed that PSG-1 could maintain the integrity of the intestinal structure by promoting the expression of goblet cells and levels of tight junction proteins in the colon of DSS-induced colitis mice. Furthermore, PSG-1 relieved the inhibition of Bcl-2 and the overexpression of caspase-3 and caspase-9 caused by DSS. Simultaneously, PSG-1 restored the expression of Atg5, Atg7 and beclin-1 and inhibited the p-akt and p-mTOR levels, suggesting that PSG-1 promoted autophagy via the Akt/mTOR pathway. Moreover, PSG-1 inhibited the content of DCs in the colon and modulated the expression of IL-10 in DCs. In conclusion, PSG-1 alleviated DSS-induced ulcerative colitis by protecting the apoptosis/autophagy-regulated physical barrier and the DC-related immune barrier.

Lipopolysaccharide (LPS)-induced inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model were established to evaluate the anti-inflammatory effect and underlying mechanism of Ganoderma atrum polysaccharides (PSG-1). It was found that PSG-1 reduced LPS-induced secretion of pro-inflammatory cytokine (TNF-α, IL-6 and IL-1β), ROS levels, and inhibited the expression of COX-2 in LPS-stimulated inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model. Furthermore, PSG-1 suppressed the LPS-induced activation of MAPKs signaling pathways, and regulated oxidative stress by activating the Nrf2/Keap1 signaling pathways. These above results indicated that PSG-1 not only has a direct anti-inflammatory effect in LPS-induced inflammatory macrophages model, but also has an indirect anti-inflammatory effect in intestinal-like Caco-2/macrophages co-culture inflammation model. These findings provide new insight of the mechanism underlying the anti-inflammatory activities of PSG-1, and facilitated the expansion of the application of PSG-1 in natural functional food., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The study aimed to investigate the protective effect and underlying mechanism of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on macrophage injury induced by acrolein. The results showed that PSG-1 restored the cell viability damaged by acrolein. In addition, PSG-1 significantly reduced the acrolein-induced occurrence of apoptosis via increase of Bcl-2 expression, mitochondrial membrane potential (MMP), decrease of ROS, cytochrome c (Cyt-C), caspase-3, caspase-9. Moreover, the overexpressions of autophagy-related proteins (LC3, Beclin-1, Atg7 and Atg5) were suppressed by PSG-1, which demonstrated that PSG-1 inhibited autophagy in acrolein treated macrophage. Beside, PSG-1 significantly elevated the expression level of p-mTOR, suggested that PSG-1 mediated autophagy through mTOR pathway. Furthermore, inhibitor of autophagy could inhibit apoptosis in acrolein-induced macrophage, suggesting that autophagy may be involved in the regulation of apoptosis. In summary, the present study demonstrated that PSG-1 protected acrolein-induced macrophage injury via autophagy-dependent apoptosis., (Copyright © 2019 Elsevier Ltd. All rights reserved.)