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Experimental Study on the Pathogenesis and Therapy of Nonalcoholic Steatohepatitis

Author: DengBin
Tutor: DaiLin
School: Dalian Medical University
Course: Internal Medicine
Keywords: Non - alcoholic steatohepatitis Insulin Resistance Lipid metabolism disorders Oxygen stress / lipid peroxidation
CLC: R575.1
Type: Master's thesis
Year: 2004
Downloads: 93
Quote: 2
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Objective: Non-alcoholic steatohepatitis (nonalcoholic steatohepatitis, NASH) incidence increased year by year, it can develop into liver fibrosis, cirrhosis and liver, end-stage disease, its pathogenesis is not clear, the lack of effective treatment. In this study, the high-fat high-cholesterol diet induced rat NASH model, serum insulin, TNFα levels, liver tissue of MDA, SOD level and insulin sensitizers intervention, in order to clarify (1) NASH onset The various stages of the existence of insulin resistance; (2) the TNFα and oxygen stress / lipid over whether oxidative damage in various stages of the pathogenesis of NASH play a role; (3) whether the insulin sensitizer impact of these factors in turn affect the formation of NASH. The completion of this study will contribute to further understanding of the pathogenesis of NASH and guide clinical treatment. Methods: 50 normal SD rats fed for one week, were randomly divided into 5 groups, normal diet control group (n = 10 rats); model group I (n = 10 rats) and model group II (n = 10) based on fed a high-fat diet (standard diet plus 13% lard, 2% cholesterol feeding), the administration of group I and administered in group II were given after four weeks and 9 weeks of pioglitazone 10mg · kg-fat feeding 1 · d-1 orally. The rats were sacrificed and the weekend of September 14 weekend, the conventional preparation of serum and liver tissue homogenates of liver tissue sections. Measuring length, weight, liver wet weight, liver index (liver wet weight / body weight × 100%) and Lee s index (weight 0.33 / body length × 1000) and other physical indicators; fasting glucose automatic biochemical analyzer (FBG), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and blood lipid levels, copper staining serum FFA levels, insulin (FBI) levels were measured by radioimmunoassay, insulin sensitivity index (ISI = 1 / FBG * FBI); enzymatic lt; WP = 5 gt; Determination of liver homogenate SOD and the MDA level; the conventional preparation HE staining histopathology, diagnosis is made by an experienced pathologist blinded reading. Results: 1.9 weeks after the model rats appear obvious insulin resistance and lipid metabolism disorders; than normal serum levels of TNFα were significantly higher; ALT, AST levels were not significantly higher; liver homogenates MDA levels, SOD levels with normal group showed no significant difference; mild to moderate steatosis and ballooning degeneration of liver tissue; Rats administered insulin resistance and lipid metabolism disorders significantly improved serum TNFα, ALT, AST levels and liver tissue of MDA SOD did not change significantly, generally normal liver tissue structure. The model rats insulin resistance and lipid metabolism disorders extent of 2.14 weeks compared with the previous significant progress; no significant progress in the serum levels of TNFα than before; serum ALT, AST levels were significantly higher than normal; liver homogenates MDA levels were significantly elevated , SOD level was significantly reduced; - severe steatosis and ballooning degeneration of liver tissue, all specimens appear lobular inflammatory cell infiltration and scattered spotty necrosis; Rats administered insulin resistance and lipid metabolism disorders are a significant improvement, serum ALT, AST levels decreased significantly, no significant changes in serum levels of TNFα, liver homogenates MDA, SOD levels of hepatic steatosis and ballooning degeneration is reduced significantly, but still see the obvious lobular inflammation cell infiltration. Conclusion: The long-term high-fat high-cholesterol diet can establish rat NASH model rat model of liver lesions show dynamic progress, the obvious pathological stage; 2. Played a key role in insulin resistance in the liver tissue steatosis does not play a major role in the process of fatty degeneration of the liver tissue lesions progress inflammatory injury; 3. applications insulin-sensitizing agent can improve the fatty degeneration of the liver tissue, but can not alleviate liver tissue inflammatory cell infiltration; oxygen stress / lipid peroxidation may further inflammatory response in the liver tissue steatosis play an important role; 5. TNFα may play a role in the pathogenesis of NASH mediated inflammatory response induced insulin resistance.

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CLC: > Medicine, health > Internal Medicine > Digestive and abdominal diseases > Liver and gall bladder disease > Hepatitis
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