The Effect Of Heme Oxygenase-1and Resistin On Pathogenesis Of Nonalcoholic Fatty Liver Disease

Objective: with the improvement of living standards, and thechange of eating habits,more and more people are suffer fromnonalcoholic fatty liver disease. Nonalcoholic steatohepatitis(NASH)accounts for an average10%of the population,especially inpatients with obesity and diabetes about50%.Nonalcoholic fattyliver disease is a common liver disease, eventually developed tocirrhosis and liver cancer.The pathogenesis of nonalcoholic fattyliver disease (NAFLD) is related with hepatic metabolismsyndrome、visceral obesity、insulin resistance、oxidative stress andinflammation connection. These factors are related withdevelopment of nonalcoholic fatty liver.This paper was aimed toinvestigate the role of Heme oxygenase-1and resistin inpathogenesis of nonalcoholic fatty liver disease (Nonalcoholicsteatohepatitis, NASH)。Methods: the60male SD rats, whichweighed (200g±20g),a week after the conventional breedingwere randomedly divided into four groups: the control group only15(ordinary feed) and nonalcoholic fatty liver disease model grouponly15, hemoglobin oxygen and enzyme inhibitor-1only15(fourweeks after high fat diet fed and then every weekend tail intravenous zinc original porphyrin inhibitor) and resistin inhibitedgroup only15(four weeks after high fat diet fed,then intragastricadminsteration of American ginseng). In fourth weekend, eighthweekend and twelfth weekend respectively,5rats were put todeath.Abdominal aortic bloods were taken for deiermination of theaspartic acid aminotransferase (AST)、alanine amino shift enzyme(ALT)、 bood fat total cholesterol (TC)、 triglycerides (TG)、tumor necrosis factor alpha (TNF a)、 high density lipoproteincholesterol (HDL-C) and low density lipoprotein cholesterol(LDL)-C). Pathological changes of the liver tissue was observedwith HE dying by light microscop. Immulogical histologicalchemisty of hemoglobin oxygen and enzyme-1was detected bylight microscopy. The positive cells percentage and coloring depthof heme oxygen and enzyme-1could show expression ofhemoglobin oxygen and enzyme-1in rat liver tissue. mRNAexpressions of resistin in rat liver tissue was detected withRT-polymerase chain reaction (PCR).Results: with severity ofnon-alcoholic fatty liver diseasese increased, levels of aspartic acidaminotransferase (AST), alanine amino shift enzyme (ALT), bloodfat total cholesterol (TC), triglycerides (TG), tumor necrosis factor(TNF a alpha, low density lipoprotein cholesterol (LDL)-C) in modelgroup changed. Hepatic pathology in model group got steatosis, necrosis and inflammation cell infiltration.in heme oxygen andenzyme inhibition-1group the liver had more serious steatosisand shading lighter color than in model group.At8th weekend,and twelfth weekend liver steatosis of nonalcoholic fat ty liverdisease was more serious in model group; in American ginsengirrigation stomach group,at eighth, twelfth weekend the changeof hepatic pathology was more decreased than in model group.Inrat liver tissue mRNA expression of the resistance in nonalcoholicfatty liver disease model group was reduced. Conclusion: hemeoxygen enzyme-1and resistance element innonalcoholic fatty liverdisease rats were higher than that in the normal group, but theireffect is different. Heme oxygen and enzyme-1can slow or stopthe progress of nonalcoholic fatty liver disease, red blood oxygenand enzyme-1(HO-1) is degradation hemoglobin generationcarbon monoxide, free iron, bravery, green key enzymes. Theproduct of hemoglobin has anti-inflammatory, antioxidation,prevention of the necrosis of liver cells,and the role of theantioxidant stress. Resistin is from fat cells,and will prevent orreduce the input of the liver glycogen which leads to insulinresistance. Resistin in obese patients increases and there is aclose relationship between visceral obesity and resistin which maybe contributied to the development of fatty liver factors. Resistin may increase the formation of nonalcoholic fatty liver disease byinsulin resistance, whereas improving insulin resistance may delaythe development of nonalcoholic fatty liver disease.