germanium and Mastitis

Ge is a trace element needed for good nutrition and health protection in animals and humans. Ge can be consumed by drinking or eating or administered by injection and transferred with the blood to exert pharmacological activities. The blood is important in the formation of milk. Mastitis is a serious health hazard in animals and humans. The present study explored the effect of Ge on mastitis and the potential underlying mechanism. A mastitis mouse model was established with LPS. mMECs were prepared for study in vitro. Histopathological changes showed that Ge had a protective effect on mammary gland tissues. Ge inhibited MPO activity to reduce inflammatory cell infiltration during mastitis. ELISA and qPCR results for tissues and cells showed that the expression of TNF-α, IL-1β, and IL-6 was decreased and that of IL-10 was increased by Ge in a dose-dependent manner in mastitis. An analysis of protein phosphorylation was performed with sandwich ELISAs for both tissues and mMECs. The results showed that Ge significantly inhibited the phosphorylation of IκB, NF-κB p65, p38, ERK, and JNK, which was dramatically increased by LPS. These results demonstrate that Ge has an inhibitory effect on inflammation that protects mammary gland tissues by inhibiting NF-κB and MAPK pathway activation and reducing TNF-α, IL-1β, and IL-6 expression. Ge may be an effective clinical treatment for mastitis and other inflammatory diseases.

Topics: Animals; Anti-Inflammatory Agents; Female; Germanium; Humans; Lipopolysaccharides; Mammary Glands, Animal; Mastitis; Mice; Mice, Inbred BALB C; NF-kappa B