Non-alcoholic fatty liver disease molecular pathogenesis of.doc

 PAGE \* MERGEFORMAT 12 Non-alcoholic fatty liver disease molecular pathogenesis of [Key Words] molecular biology of non-alcoholic liver disease pathogenesis Non-alcoholic fatty liver disease (nonalcoholic fatty liver disease, NAFLD) is no history of excessive drinking (alcohol intake lt;20 g / d) and hepatic steatosis, ballooning degeneration, mild diffuse lobular inflammation and (or) hepatic central vein, sinusoidal collagen deposition around the clinical and pathological features such as chronic liver disease [1], which includes simple fatty liver (nonalcoholic fatty liver, NAFL), steatohepatitis (nonalcohlic steatohepatitis, NASH), fatty cirrhosis (fatty liver cirrhosis, FLC) of three types. NAFLD has become the leading cause of abnormal ALT result, and some patients progress to end-stage liver disease, and even some patients with liver tumors. At present the incidence of NAFLD my region is gradually increased [2], because the incidence of the disease is not entirely clear that the occurrence of insulin resistance, oxidative stress response and lipid peroxidation metabolism imbalance [3]. In this paper, the molecular biology in recent years the disease Some Progress on study areas are summarized below. 1. Oxygen free radicals on the role of liver cell damage Because patients with triglyceride accumulation in liver cells, a large number of free fatty acids (FFA oxidation in the mitochondria, resulting in excessive superoxide anion and reactive oxygen species (reactive oxygen species, ROS), the antioxidant depletion, excessive hydrogen peroxide (H2O2) and hydroxide ions (OH) damage the liver cells, mitochondria and cell membrane, so that the normal liver cell growth arrest, inflammation, degeneration, eventually leading to liver cell necrosis causing clinical symptoms [4]. Oxygen is the maintenance of biological activity of essential elements, but its metabolic intermediates formed during the ROS, and the phospholipid membrane, membrane recepto