4.7 Article

Artemether Attenuates Gut Barrier Dysfunction and Intestinal Flora Imbalance in High-Fat and High-Fructose Diet-Fed Mice

Journal

NUTRIENTS
Volume 15, Issue 23, Pages -

Publisher

MDPI
DOI: 10.3390/nu15234860

Keywords

artemether; metabolic disorder; gut microbiota; intestinal barrier dysfunction; inflammation

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This study investigates the potential mechanism of Artemether (ART) in diet-induced intestinal injury. The results suggest that ART intervention may alleviate intestinal barrier function disorders and inflammatory responses by restoring intestinal flora balance, increasing the expression of tight junction proteins, and decreasing the expression of pro-inflammatory factors. Moreover, ART intervention inhibits the activation of the TLR4/NF-kappa B p65 pathway in colon tissue, indicating a potential protective effect of ART on intestinal inflammation.
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-alpha and IL-1 beta. Moreover, ART intervention restrained HFHF-induced activation of the TLR4/NF-kappa B 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.

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