Therefore, analysis using the nested PCR products from small amounts of biopsy specimens may not be suitable for quantifying F. varium in UC patients. Other pathogens besides F. varium may also be associated with the pathogenesis of UC. As these three antibiotics used for the ATM therapy are lethal to many bacterial species, unidentified pathogens could be more significantly decreased by the ATM therapy. In conclusion, the mucosa-associated bacterial components analyzed by T-RFLP are useful to assess the alteration of the intestinal microbiota in UC after ATM therapy. The ATM antibiotic combination regimen significantly altered intestinal microbiota in UC patients compared to the placebo group. Our study supports the association of microbial agents with the pathogenesis of UC. A limitation of our study is the relatively small sample size. Further studies are needed to evaluate the clinical significance of long-term alteration of intestinal microbiota in UC patients treated with ATM. Autophagy is a highly conserved cellular process in eukaryotic cells involved in Forsythin protein, lipid, and organelle degradation via the lysosomal pathway. Autophagy begins with the formation of double-membranous structures called phagophores, which elongate and engulf portions of the cytoplasm to form autophagosomes. Subsequently, autophagosomes fuse with lysosomes to form autophagolysosomes, where the engulfed contents are degraded by acidic lysosomal hydrolases. Autophagy is involved in cell growth, survival, development, and cell death. Impaired autophagic flux has been associated with pathologic neurologic, musculoskeletal, immunologic, cardiovascular, and hepatic conditions. The liver is one of the most important metabolic organs, and is highly dependent on autophagy for both normal function and protection against hepatic diseases such as non-alcoholic fatty liver disease, viral hepatitis, and fibrotic disorders. During periods of starvation, autophagy degrades cytoplasmic components to produce amino acids and fatty acids that can be used to synthesize new proteins or generate ATP for cell survival. Additionally, there is considerable evidence that impaired autophagy contributes to a number of common hepatic diseases, including tissue injury due to toxins, high-fat-diet, ischemia/reperfusion, and viral hepatitis, as well as hepatocellular carcinoma. Epigallocatechin-3-gallate is the most abundant polyphenol in green tea and has been thought to be responsible for most of latter’s therapeutic benefits. In particular, EGCG has anti-steaototic 10-Gingerol effects on the liver. Autophagy also has been shown to be involved in these beneficial effects. Currently, it is not known whether EGCG regulates hepatic autophagy. Given both the importance of hepatic autophagy and the beneficial effect of EGCG on pathologic liver conditions, we investigated whether EGCG regulates autophagy and lipid clearance in the liver. Recently, there have been several reports suggesting that some of the beneficial effects of EGCG may be mediated by regulation of autophagy. However, the effects of EGCG on autophagy seem to be tissue-specific. In macrophages, EGCG promotes autophagic degradation of endotoxin-induced HMGB1, a late lethal inflammatory factor. The autophagy-promoting effect of EGCG also occurs in bovine aortic endothelial cells, and accounts for its reduction of lipid accumulation. However, in human retinal pigment epithelial cells, EGCG reduces 
UVB lightinduced retinal damage by down-regulation of autophagy. Although EGCG also is protective against liver injury, it is not known whether it regulates hepatic autophagy to mediate these effects.