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目的研究脂多糖(lipopalysaccharide,LPS)预处理对高糖商脂膳食诱导的非酒精性脂肪性肝炎(nonalcoholic steato-hepatitis,NASH)的影响及血浆脂联素(adiponectin,APN)表达的变化。方法 24只Wistar雄性大鼠随机分为正常对照组、LPS预处理组和肝损伤组。肝损伤组饲以高糖高脂饲料;LPS预处理组饲料同肝损伤组,隔日皮下注射LPS0.5mg/kg;正常对照组饲以普通饲料;所有大鼠自由进食与饮水。于实验第9周末处死动物。制备肝组织切片,计数浸润肝组织的淋巴细胞;测定血浆内毒素(endotoxin,ET)水平和丙氨酸转氨酶(alanine aminotransferase,ALT)活性、肿瘤坏死因子-α(tumor necrosisfactor-α,TNF-α)、APN含量。结果肝损伤组血浆ET水平与正常对照组相比显著升高;LPS预处理组血浆ALT水平、肝组织淋巴细胞计数与肝损伤组比较均显著降低;血浆TNF-α水平LPS预处理组与肝损伤组比较明显降低,而血浆APN则相反,经统计学分析差异均有统计学意义(P<0.05)。肝组织切片HE染色结果显示,LPS预处理组与肝损伤组相比,肝细胞内脂肪空泡小、数量少,脂肪变性明显减轻。结论 LPS预处理可以减轻高糖高脂膳食诱导的NASH,其机制可能与高水平的脂联素抑制TNF-α的产生,从而降低TNF-α介导的肝细胞损害有关。
Objective To investigate the effects of lipopolysaccharide (LPS) preconditioning on nonalcoholic steato-hepatitis (NASH) and plasma adiponectin (APN) expression induced by high glucose and fat diet. Methods Twenty-four Wistar male rats were randomly divided into normal control group, LPS preconditioning group and liver injury group. The rats in the liver injury group were fed with high-sucrose and high-fat diet. LPS pretreatment group and liver injury group were injected subcutaneously with LPS 0.5 mg / kg every other day. The normal control group was fed with normal diet. All rats were fed and drinking freely. Animals were sacrificed at the end of the 9th week of experiment. The liver tissue sections were prepared and the lymphocytes infiltrating the liver tissue were counted. The level of plasma endotoxin (ET) and the activity of alanine aminotransferase (ALT), tumor necrosis factor-α (TNF-α) ), APN content. Results Compared with normal control group, the level of plasma ET in liver injury group was significantly higher than that in normal control group. The levels of ALT and LPS in liver injury group were significantly lower than those in liver injury group. The levels of TNF- The injury group was significantly reduced, while the plasma APN was the opposite, statistically significant differences were statistically significant (P <0.05). Hematoxylin-eosin staining showed that compared with the liver injury group, the LPS pretreatment group had less fat vacuoles and a small number of hepatocytes, and the fatty degeneration was significantly reduced. Conclusions LPS pretreatment can reduce the NASH induced by high glucose and high fat diet. The mechanism may be related to the inhibition of TNF-α production by high levels of adiponectin and the decrease of TNF-α-mediated hepatocellular damage.