Differences between NAFLD and ALD or the different extent of damage in ALD might support the supposed functional involvement of PAI-1 in progression of ALD. Similarly interesting would be if expression of the adiponectin receptor ApoRII in the liver tissue correlates with severity of cirrhosis. Another limiting Compound-K aspect is the relatively small number of NAFLD patients. This is partially due to the intention of comparing physiological similar patients with NAFLD 
and ALD. As the majority of definite NAFLD patients are obese, restriction to BMI of below 30 reduced the available number of patients. Finally, one limitation is represented by missing follow ups on the patients to assess development, progression or recession of the liver damage during disease course. Taken together it could be shown that adipokines/cytokines may serve as Atropine sulfate markers for identification of NAFLD vs. ALD. This would enable clinicians to cross-check the information given by patients about their alcohol consumption with minor additional expenses but with high accuracy. In addition, severity of ALD may be non-invasively diagnosed via serum cytokine concentrations. Adiponectin or its receptors might even exhibit functional and thus therapeutic relevance in the progression of ALD to cirrhosis. It has been reported that A. annua contained a significant level of phenolic compounds including luteolin, luteolin-7-glucoside, kaempferol, quercetin, rutin, coumarin and so on. The present study also showed that the ethanol extract of the herb contained 32.6762.84 mg total phenolics per g dry matter, consistent with the previous report that the herb had 1.54 mg total phenolics per g fresh weight. The present study confirmed antioxidant activity of 80%ethanol extract of the herb in cultured cell and mouse model systems. The serum level of 8-OH-dG increased by D-galactose injection was restored to the untreated control level by feeding diet containing AA extract. The D-galactose exposure has been reported to induce an increase in peripheral oxidative stress, including an increase in malondialdehydeand decreases in total antioxidative capabilities, total superoxide dismutase, and glutathione peroxidase activities. Our study also confirmed that the MDA and 8-OH-dG levels were significantly enhanced by D-galactose in mouse and were decreased upon treatment with either a-tocopherol or AA extract. A chronic administration with a low dose of D-galactose is reported to induce changes that mimics natural aging in animals, such as a shortened life span, cognitive dysfunction, neurodegeneration, and oxidative stress. The protective effect of AA extract from lipid peroxidation and DNA damage appears to be associated with the capability of AA extract to induce antioxidant enzymes including NQO1. That is, it was well established that antioxidant enzymes were induced by some phytochemicals in an Nrf2-mediated fashion. More specifically, some electrophiles including sesquitepenes interact with Keap1 that is present in heterodimeric form with Nrf2 in cytosol, releasing Nrf2 from the complex. The released Nrf2 migrates into the nucleus and act as a transcriptional factor, promoting expression of antioxidant enzymes such as NQO1, heme oxygenase 1, glutathione reductase, c-glutamyl cysteine ligase, and glutathione S-transferase and so on. The current study also demonstrated that AA extract increased the NQO1 activity and expression in mouse organs such as stomach, small intestine, and large intestine, and kidney.