Basic & Clinical Medicine ›› 2012, Vol. 32 ›› Issue (10): 1154-1160.

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AMPK expression decreases in alcoholic liver disease

  

  • Received:2011-09-20 Revised:2012-01-05 Online:2012-10-05 Published:2012-09-28

Abstract: 【Abstract】 Objective To observe the effects of ethanol consumption on the expression of AMP-activated protein kinase(AMPK) in the rats hepatic tissue with alcoholic liver disease(ALD). Methods In the 50 male Wistar rats, 10 rats were randomly assigned to the normal control group. Others were to develop the rats model of ALD by intragastric alcohol and sacrificed randomly at the end of 4th, 8th, 12th and 16th week, and the serum and liver samples were collected respectively. The contents of ALT, AST, CHE, TG, TC, LDL, VLDL, HDL in serum were examined and the pathological changes were observe in liver tissue by HE, Sirius red.and Sudan Ⅳ. And the protein expression of AMPK, Acetyl-CoA carboxylase (ACC), Sterol regulatory element-binding proteins (SREBP) and mRNA were detected by immunohisto-chemical staining and RT-PCR respectively. Results With the consumption of ethanol , the level of ALT and AST in the serum increased while the CHE decreased gradually. The level of TG, TC, LDL, VLDL in the serum increased while the HDL decreased gradually. Compared with the control group, the expression of AMPK in model group decreased gradually with the progress of ALD, and it negatively correlated with the expression of ACC and SREBP of hepatic tissue(r=-0.911and -0.907 respectively, P<0.01). Conclusions The expression of AMPK in hepatic tissue was decreased with the process of ALD, which inhibit the activation to ACC and SREBP. It causes the increase of lipid synthesis, which would result in the fat accumulation in the liver and has a great effect on the liver injury. As a new pharmacological target, AMPK provides a new idea for the prevention and treatment of ALD.

Key words: AMP-activated protein kinase, Acetyl-CoA carboxylase, Sterol regulatory element-binding proteins, Alcoholic liver disease, Oxidative stress, Lipid metabolism