Alcoholic liver disease (ALD) refers to the damages to the liver and its functions due to alcohol overconsumption. It consists of fatty liver/steatosis, alcoholic hepatitis, steatohepatitis, chronic hepatitis with liver fibrosis or cirrhosis, and hepatocellular carcinoma. However, the mechanisms behind the pathogenesis of alcoholic liver disease are extremely complicated due to the involvement of immune cells, adipose tissues, and genetic diversity. Clinically, the diagnosis of ALD is not yet well developed. Therefore, the number of patients in advanced stages has increased due to the failure of proper early detection and treatment. At present, abstinence and nutritional therapy remain the conventional therapeutic interventions for ALD. Moreover, the therapies which target the TNF receptor superfamily, hormones, antioxidant signals, and MicroRNAs are used as treatments for ALD. In particular, mesenchymal stem cells (MSCs) are gaining attention as a potential therapeutic target of ALD. Therefore, in this review, we have summarized the current understandings of the pathogenesis and diagnosis of ALD. Moreover, we also discuss the various existing treatment strategies while focusing on promising therapeutic approaches for ALD.

Background/Aim: Colon cancer is the second most common deadliest malignancy in the world and better understanding of its underlying mechanisms is needed to improve clinical management. Natural plant extracts are gaining attention in the development of new therapeutic strategies against various cancer types. Shikonin is a naturally extracted naphthoquinone pigment with effects against cancer, including colon cancer. Materials and Methods: In this study, we conducted a series of in vitro experiments to show the effects of Shikonin on colon cancer cell apoptosis. A colon cancer cell line with overexpression of peroxiredoxin V (PrxV) was constructed and the relationship of PrxV expression with Shikonin-induced cell apoptosis was investigated. Results: Shikonin induced colon cancer cell apoptosis via regulation of mammalian target of rapamycin signaling. Shikonin-induced cell apoptosis was abrogated by overexpression of PrxV. Conclusion: According to the results obtained in this study, targeting PrxV may provide new insight for the successful management of colon cancer by inducing cell apoptosis.

Background: Peroxiredoxin II (PRDX2) performs unique roles in cells. It can reduce peroxides through cysteine residues, and helps prevent the effects of oxidative stress on cells. It is closely related to the occurrence and development of various diseases, especially alcoholic liver injury and even liver cancer. The metabolism of alcohol in hepatocytes leads to the increase in the levels of reactive oxygen species (ROS), oxidative stress, injury, and apoptosis. Therefore, this study focused on the investigating the protection conferred by PRDX2 against alcohol-induced apoptosis of hepatocytes. Materials and Methods: PRDX2 inhibition of alcohol-induced apoptosis in L02 hepatocytes was analyzed by 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, fluorescence microscopy, flow cytometry, western blotting and hematoxylin and eosin staining. Results: The results showed that the levels of reactive oxygen species, protein kinase B, β-catenin, B-cell lymphoma-2 (BCL2), BCL-XL, BCL2-associated X, cleaved caspase-3, and cleaved poly (ADPribose) polymerase in PRDX2-silenced cells were increased significantly after the treatment of cells with ethanol. Similar results were obtained in an in vivo Prdx2-knockout mouse model of alcoholic liver injury. Therefore, PRDX2 may regulate the phosphorylation of the AKT signal protein by eliminating reactive oxygen species from cells, and it inhibits the downstream mitochondria-dependent apoptosis pathway, and, thereby, the apoptosis of cells. Conclusion: Thus, PRDX2 may be a potential molecular target for the prevention and treatment of alcoholic liver injury.The relationship between alcohol and health has always been a research topic of great concern. Alcohol intake is associated with injury to organs, cancer, cardiovascular diseases, cirrhosis, and other diseases, especially liver damage, and can, therefore, be a direct or indirect cause of death (1). Alcoholic liver disease has become one of the main diseases threatening human health because of its complicated pathogenesis, subjective dependence, and social issues (2). In 2010, nearly 50% of the world's population was drinking alcohol in some or other, and more than one million deaths worldwide were attributed to cirrhosis, with 47.9% of those who died had a long history of alcohol abuse (3). In 2012, 5.9% of deaths globally were related to alcohol abuse. Among long-term alcoholics, 80-90% suffer from alcoholic fatty liver, 20-40% develop liver fibrosis, disease in 8-20% progresses to cirrhosis and ascites, and 3-10% develop hepatocellular carcinoma (4).Alcoholic liver disease begins with steatosis, which is characterized by the rise of triglycerides in the liver. The histological features of advanced alcoholic liver disease are necrosis and apoptosis of hepatocytes, and are important features of alcoholic liver disease in clinical practice (5). Early studies on the pathogenesis of alcoholic liver disease mainly

Background/Aim: Staphylococcus aureus (S. aureus) is a major gram-positive pathogen, which can cause toxic and immunogenic injuries both in nosocomial and community-acquired infections. Peroxiredoxin (Prx) I plays crucial roles in cellular apoptosis, proliferation, and signal transduction as well as in immunoregulation. The present study aimed to investigate whether Prx I protects mice from death caused by the heat-killed Staphylococcus aureus. Materials and Methods: In the present study, we challenged the wild-type and Prx I-deficient mice with heat-killed S. aureus (HKSA). The effects of Prx I were evaluated by a series of in vitro and in vivo experiments including western blot, Haematoxylin and Eosin staining, splenocyte analysis and cytokines analysis. Results: Intra-peritoneal (ip) inoculation of HKSA resulted in increased mortality of Prx I-knockout (KO) mice with severe liver damage and highly populated spleens with lymphocytes. Furthermore, HKSA infections also bursted the production of both pro-inflammatory and antiinflammatory serum cytokines in Prx I KO compared to wildtype mice. Conclusion: Enhanced mortality of S. aureusinfected mice with Prx I deficiency suggested that Prx I may protect against the infection-associated lethality of mice. Peroxiredoxin (Prx) I, an antioxidant enzyme, belongs to 2-cysteine Prxs (1). Recent evidence shows that Prx I participates in several cellular signaling pathways by interacting with diver proteins to regulate cell differentiation, apoptosis and proliferation (2-4). Accumulation of reactive oxygen species (ROS) in cells can cause oxidation of DNA, membrane lipids and proteins, resulting in increased cellular damage (5). Prx I plays an important role in scavenging ROS in cells (6). In the last decade, the regulatory role of Prx I in tumorigenesis has been well defined both in vivo and in vitro. Depletion of Prx I can spontaneously induce the development of several malignant cancers and severe haemolytic anaemia, as well as oxidative DNA damage and decreased cell proliferation (7). Furthermore, a previous study by our group has also shown that Prx I suppresses the K-ras-induced lung carcinogenesis via the ROS/ERK/cyclin D1 signaling pathway (8), suggesting that Prx I may be a tumor suppressor that could prevent carcinogenesis.