The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is a bioactive compound found in cruciferous vegetables; however, it has not been reported whether SFN improves NAFLD via the gut–liver axis. C57BL/6 mice were fed a high-fat and high-fructose (HFHFr) diet, with or without SFN gavage at doses of 15 and 30 mg·kg⁻¹ body weight for 12 weeks. The results showed that SFN reduced weight gain, hepatic inflammation, and steatosis in HFHFr mice. SFN altered the composition of gut microbes. Moreover, SFN enhanced the intestinal tight junction protein ZO-1, reduced serum LPS, and inhibited LPS/TLR4 and ERS pathways to reduce intestinal inflammation. As a result, SFN protected the intestinal integrity and declined the gut-derived LPS translocations to the liver in HFHFr diet-induced mice. SFN decreased the liver LPS levels and inhibited the LPS/TLR4 pathway activations, thus inhibiting the pro-inflammatory cytokines. Notably, Spearman correlation analysis showed that the protective effect of SFN on intestinal barrier integrity and its anti-inflammatory effect on the liver was associated with improved intestinal dysbiosis. Above all, dietary intervention with SFN attenuates NAFLD through the gut–liver axis.

The trypsin inhibitor (TI) is one of the most important anti-nutritive elements in soybeans. As a new nonthermal technology, dielectric-barrier discharge (DBD) cold plasma has attracted increasing attention in food processing. In this research, we investigated the effect of dielectric-barrier discharge (DBD) plasma treatment on soybean trypsin inhibitor content and its structure, evaluated TI toxicity and the safety of its degradation products after treatment with DBD technology in vitro and in vivo, and applied the technology to soybean milk, which was analyzed for quality. Using the statistical analysis of Student’s t-test, the results demonstrated that DBD plasma treatment significantly decreased the content of TI (33.8 kV at 1, 3, or 5 min, p < 0.05, p < 0.01, p < 0.001) and destroyed the secondary and tertiary structures of TI. TI was toxic to Caco-2 cells and could inhibit body weight gain, damage liver and kidney functions, and cause moderate or severe lesions in mouse organ tissues, whereas these phenomena were alleviated in mice treated with degradation products of TI after DBD plasma treatment under the optimal condition (33.8 kV at 5 min). The content of TI in DBD-treated soymilk was also significantly reduced (p < 0.001), while the acidity, alkalinity, conductivity, color, and amino acid composition of soymilk were not affected, and there were no statistical differences (p > 0.05). In summary, DBD plasma is a promising non-thermal processing technology used to eliminate TI from soybean products.

Intestinal inflammation is a key determinant of intestinal and systemic health, and when our intestines are damaged, there is disruption of the intestinal barrier, which in turn induces a systemic inflammatory response. However, the etiology and pathogenesis of inflammatory diseases of the intestine are still not fully understood. Artemether (ART), one of the artemisinin derivatives, has been widely used to treat malaria. Nevertheless, the effect of ART on intestinal inflammation remains unclear. The present study intended to elucidate the potential mechanism of ART in diet-induced intestinal injury. A high-fat and high-fructose (HFHF) diet-induced mouse model of intestinal injury was constructed, and the mice were treated with ART to examine their role in intestinal injury. RT-qPCR, Western blotting, immunohistochemical staining, and 16S rRNA gene sequencing were used to investigate the anti-intestinal inflammation effect and mechanism of ART. The results indicated that ART intervention may significantly ameliorate the intestinal flora imbalance caused by the HFHF diet and alleviate intestinal barrier function disorders and inflammatory responses by raising the expression of tight junction proteins ZO-1 and occludin and decreasing the expression of pro-inflammatory factors TNF-α and IL-1β. Moreover, ART intervention restrained HFHF-induced activation of the TLR4/NF-κB p65 pathway in colon tissue, which may be concerned with the potential protective effect of ART on intestinal inflammation. ART might provide new insights into further explaining the mechanism of action of other metabolic diseases caused by intestinal disorders.