Aspergillus cristatus attenuates DSS-induced intestinal barrier damage through reducing the oxidative stress, regulating short-chain fatty acid and inhibiting MAPK signaling pathways

曲霉通过降低氧化应激、调节短链脂肪酸和抑制MAPK信号通路减轻DSS引起的肠道屏障损伤

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作者:Xin Wang, Xuejun Zeng, Xiao Zhang, Jianping Wei, Yuxiang Zhang, Fangyu Long, Tianli Yue, Yahong Yuan

Background

Probiotics are regarded as a promising strategy for relieving colitis caused by dextran sulfate sodium (DSS). One of the dominant probiotic fungi in Fuzhuan brick tea is identified as Aspergillus cristatus, but whether it can effectively improve colitis remains poorly understood. Here, the improving effect of A. cristatus on colitis was investigated.

Conclusion

Together, A. cristatus can attenuate DSS-induced intestinal barrier damage through reducing the oxidative stress, regulating SCFA and inhibiting MAPK signaling pathways (P38/JNK/ERK). Our findings indicate that A. cristatus replenishment has potential as a new probiotic fungi to reduce DSS-induced colitis. © 2022 Society of Chemical Industry.

Results

Our results showed that A. cristatus intervention prominently alleviated gut damage as evidenced by the inhibition of shortened colon length, goblet cell depletion, and histological injury. Mechanistically, after administration with low concentrations of A. cristatus H-1 and A. cristatus S-6, the expression of interleukin-6, tumor necrosis factor-α, interleukin-1β, nitric oxide, and malondialdehyde were significantly downregulated, and the content of glutathione, catalase, interleukin-10, immunoglobulin G, claudin-1, occludin, and zonula occludens-1 were effectively upregulated. More importantly, live A. cristatus supplementation lightened DSS-induced gut barrier damage by suppressing activation of the mitogen-activated protein kinase (MAPK) signaling pathway, increasing the synthesis of short-chain fatty acids (SCFAs) and stimulating the increase in peroxisome proliferator-activated receptor γ expression.

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