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.

Mare milk (MM) and fermented mare milk (FM) are specialized animal milks with high nutritional value, containing a variety of functionally active substances that are capable of resisting inflammatory responses and oxidative stress. However, researches on the maintenance of intestinal homeostasis have been insufficient. This study aimed to investigate the effects of MM and FM on the prevention of DSS-induced ulcerative colitis in a mouse model and to preliminarily elucidate the underlying mechanisms. The results showed that MM and FM had different degrees of protective effects against the damage of DSS and alleviated ulcerative colitis by inhibiting weight loss, reducing colon length shortening, and restoring intestinal structure. Additionally, MM and FM maintained intestinal tight junction protein levels to repair barrier function, downregulated inflammatory cytokines (e.g., IL-1β, TNF-α, IL-6, and iNOS) and bolstered the body's antioxidant defense system. Moreover, MM and FM regulate the dysregulation of intestinal microenvironment by improving gut microbiota diversity and reshaping its structure, including increasing the proportion of Firmicutes and Bacteroidetes and the relative abundance of beneficial bacterial genera (e.g., Akkermansia). In summary, mare milk and fermented mare milk can serve as a dietary resource for preventing ulcerative colitis and maintaining intestinal homeostasis.

Background/Objectives: The global prevalence of obesity and its associated health complications represent significant public health concerns. Plant polysaccharides have been demonstrated to possess a range of beneficial pharmacological effects. This experiment was designed to elucidate the mechanisms of dietary Taraxacum mongolicum polysaccharides involved in the regulation of obesity and fat browning. Methods: Male C57BL/6J mice were randomly divided into three groups: a control group, a high-fat diet (HFD) group, and an HFD group supplemented with 0.3% TMPs. The mice were fed their respective diets for 10 weeks, after which their body weight, food consumption, and serum lipid levels were measured. Histological analysis was performed to assess lipid deposition in adipose tissue and liver. Western blot was used to assess the expression of proteins involved in the AKT/mTOR pathway. Results: The results show that compared with the HFD group, the TMP supplementation group’s body-weight gain (12.17 ± 1.77) significantly decreased. TMPs also reduced serum levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Histological analysis showed that TMPs reduced lipid deposition in both adipose tissue and the liver. Conclusions: In addition, TMPs increased the expression of phosphorylated AKT and the mechanistic target of rapamycin (mTOR), indicating that TMPs exert their beneficial effects on lipid metabolism via the AKT/mTOR pathway.