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Objective: rat fat diet for eight weeks after intraperitoneal injection of small doses of endotoxin, while I emodin intervention to understand the impact of endotoxin on the development of non-alcoholic fatty liver disease (nonalcholic fatty liver disease NAFLD) and emodin possible intervention role, to provide experimental basis for clinical application emodin treatment of NAFLD. Methods: 42 male Sprague-Dawley rats were adaptive feeding one week after randomly divided into normal group (A) 34 8 and hyperlipidemia model group (M group), group A to a normal diet, B group I fat diet. After 8 weeks, the M group rats were randomly selected, whichever HE staining confirmed fatty liver change, the the A rats continued to be fed with normal diet; remaining M group, 32 rats were randomly divided into high fat group (B), fat NS group (C), the fat LPS group (D) and rhubarb intervention group (E) 8 each are to continue to the high fat diet, C group were injected intraperitoneally NS group D, E group to intraperitoneal injection of LPS lipopolysaccharide (LPS), a dose of 20ug/100g every other day for the first injection, E group I emodin 30mg/kg/d; said two weeks, 10 weeks, liver weight, liver index pathological changes in liver tissue the grading calculation of the degree of hepatic steatosis and liver inflammation grading, serum alanine aminotransferase (alanine aminotransferase ALT), aspartate aminotransferase (aspartate aminotransferase AST), serum cholesterol (total cholesterol TC), triglycerides (total cholesterol TG), low-density lipoprotein (low-density lipoprotein LDL), high density lipoprotein cholesterol (high-density lipoprotein HDL) level, liver homogenates measured malondialdehyde (Malondialdehyde MDA), superoxide dismutase the level of the enzyme (superoxide dismutase SOD), Immunohistochemical detection of liver tumor necrosis factor (tumor necrosis factor alpha TNF-a) expression of nuclear factor kB (Nuclear factor-KB NF-kB). Results: 10 weekend successfully copied rat NAFLD model. 1 weight comparison: B, C, D rats weight increase than group A (p lt; 0.05); difference in weight between the B, C, D group was not statistically significant (p gt; 0.05). Over 2 indicators: B, C, D group liver index, the degree of steatosis, inflammatory degree of serum ALT, AST levels higher than those in group A (p lt; 0.05, p lt; 0.01); D group than in the C cyanosis higher (p lt; 0.01, p lt; 0.05); E group than in the group D have to reduce (p lt; 0.01). 3 Comparison of lipid parameters: B, C, D groups in rat serum TC, TG, LDL was significantly higher than that in group A (p lt; 0.01) HDL lower than that in group A (p lt; 0.01); group D blood TC, TG, LDL were significantly higher compared with group C (p lt; 0.05, p lt; 0.01) HDL significantly reduce (p lt; 0.01); E group blood TC, TG, LDL lower than Group D (p lt; 0.05, p lt; 0.01 ) HDL increased (p lt; 0.01). 4, liver homogenate SOD MDA value comparison: B, C, D group SOD levels lower than group A (p lt; 0.05), MDA increased (p lt; 0.01); D group SOD levels compared with the C group was significantly lower (p lt; 0.01) MDA level was significantly higher (p lt; 0.01); SOD in group E compared to the elevated levels compared with group D (p lt; 0.01) MDA level compared with group D compared liters reduce (p lt; 0.01). 5 Immunohistochemistry detection of NF-κB and TNF-a comparison: B, C, D group liver: NF-κB, TNF-a enhanced expression than group A (p lt; 0.01, p lt; 0.05); D group than in the C group was significantly enhanced (p lt; 0.05, p lt; 0.01); compared to group E and group D expression diminished (p lt; 0.01, p lt; 0.05). Conclusion: 1 endotoxin induced the NAFLD liver tissue TNF-a and lipid peroxidation generate, aggravate NAFLD liver injury. 2 emodin possible through the inhibition of NF-κB activation, blocking the conduction of endotoxin damage signaling pathways, thereby slowing the pathological process of NAFLD.
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