Effects of Water Extract from Artemisia argyi Leaves on LPS-Induced Mastitis in Mice

SIMPLE SUMMARY: Mastitis is a common disease in dairy cows. On the one hand, it will reduce milk yield and milk quality of dairy cows, thus increasing the cost of animal husbandry, and, on the other hand, it will influence the health of infected animals and even human beings. Generally speaking, because mastitis is caused by pathogenic microorganisms, antibiotic treatment is commonly used. However, antibiotic resistance of microorganisms caused by wrongful use of antibiotics and antibiotic residues after treatment has become an urgent problem to be solved. Chinese herbal medicines are pure natural substances, and many of them have antibacterial, anti-inflammatory, or immune-enhancing effects. In this experiment, Artemisia argyi (A. argyi) was selected as the research object to construct the cell model of cow mastitis. Studies have found that A. argyi extract can play a positive role in the regulation of inflammation, which is rich in organic acids and flavonoids. Therefore, A. argyi extract may be a potential treatment for mastitis. ABSTRACT: In the context of the unsatisfactory therapeutic effect of antibiotics, the natural products of plants have become a research hotspot. Artemisia argyi (A. argyi) is known as a traditional medicine in China, and its extracts have been reported to have a variety of active functions, including anti-inflammatory. Therefore, after establishing the mouse mastitis model by lipopolysaccharide (LPS), the effects of A. argyi leaves extract (ALE) were evaluated by pathological morphology of the mammary gland tissue, gene expression, and serum oxidation index. Studies have shown that ALE has a restorative effect on LPS-induced mammary gland lesions and significantly down-regulated the rise of myeloperoxidase (MPO) induced by LPS stimulation. In addition, ALE played a positive role in LPS-induced oxidative imbalance by restoring the activities of glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) and preventing the increase in nitric oxide (NO) concentration caused by the over-activation of total nitric oxide synthase (T-NOS). Further analysis of gene expression in the mammary gland showed that ALE significantly down-regulated LPS-induced up-regulation of inflammatory factors IL6, TNFα, and IL1β. ALE also regulated the expression of MyD88, a key gene for toll-like receptors (TLRs) signaling, which, in turn, regulated TLR2 and TLR4. The effect of ALE on iNOS expression was similar to the effect of T-NOS activity and NO content, which also played a positive role. The IκB gene is closely related to the NF-κB signaling pathway, and ALE was found to significantly alleviate the LPS-induced increase in IκB. All of these results indicated that ALE may be considered a potential active substance for mastitis.