The Publication:

Emodin attenuates systemic and liver inflammation in hyperlipidemic mice administrated with lipopolysaccharides

Sounds like a mouthful? Don’t worry—there’s a summary below.

Publication Summary:

Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat is stored in liver cells for reasons other than heavy alcohol use. It's a broad term that describes liver conditions ranging from simple fatty liver to a more serious condition known as non-alcoholic steatohepatitis (NASH). While simple fatty liver or steatosis is usually benign and doesn't progress to cause liver damage in most people, NASH is characterized by inflammation and liver cell damage, in addition to fat in the liver, and Inflammation and liver cell damage can cause fibrosis, or scarring, of the liver, eventually leading to cirrhosis and liver cancer. Therefore, prevention of the transition from simple steatosis to NASH is critical. In this study, we aimed to test if a Chinese herb-derived compound, emodin, could halt the simple steatosis to NASH transition in a mouse model. Low density lipoprotein receptor knockout (LDLR-/-) mice were fed a western-type diet for 10 weeks to induce hyperlipidemia and fatty liver; and during the last four weeks, the mice were intra-peritoneally injected daily with lipopolysaccharides (LPS) to trigger NASH, some of the mice were injected with emodin as well to examine if emodin could attenuate NASH. Our data showed that emodin ameliorated systemic inflammation, reduced inflammatory cell infiltration in the liver, and attenuated liver function impairment. Cell culture experiments showed that emodin inhibited LPS-induced expression of proinflammatory cytokines in macrophages through suppressing Erk1/2 and p38 activation. In conclusion, emodin inhibited the transition from simple steatosis to NASH in hyperlipidemic mice challenged with LPS through suppressing systemic and macrophage inflammation. Emodin may be developed as a therapy for NAFLD.