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Nonalcoholic fatty liver disease (NAFLD) is one of the common chronic liver disease, and may turn to cirrhosis of the liver or liver cancer, but its pathogenesis is unclear.Acanthoic acid (AA) have some improvement on druginduced liver fibrosis, but its protective effect on LieberDeCarli (LD) liquid type fat dietinduced liver cell damage had less been reported, this study was conducted to determine whether acanthoic acid (AA) would ameliorate LDstimulated fatty liver in mice.Male C57BL/6 mice were randomly divided into six groups, including normal group, AA (40 mg· kg1) single group, LDtreated group, AA (20 mg· kg1) plus LDtreated group,and AA (40 mg · kg1) plus LDtreated group and protive control group, they were given LD (20mL/only), at same time garage administration AA (20 mg · kg1,40 mg· kg1), while normal group were given normal diet.Mter 8 weeks, weighed again, then took blood by removalling eyeball, took liver.The serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG) and high density lipoprotein cholesterol (HDLC) in serum were determined with reagent strips.The liver was used to do Western blot, Hematoxylin &Eosin(H&E) staining and Oil red staining.The Reagent results showed that administration of AA significantly inhibit the increase of AST, ALT caused by NAFLD, as well as TG and HDLC in serum.Supplement of AA prevented LDinduced acidophilic necrosis, increased hepatocyte muclei and stromal inflammation infiltration as indicated by liver histopathological studies.The results indicated that AA significantly decreased the expression of SREBP1, αSMA, collagenⅠ, NFκB.In addittion, TIMP1 and MMP13 kept a dynamic equilibrium, TIMP1 was decreased,while the expression of MMP13 was increased.H&Estaing and oil staing indicated that model group showed typical fatty degeneration, while the fatty liver histopathology of administration group showed significant improvement.These effects were associated with the downregulation of SREBP1 and particularly the activation of AMPK.All of these findings demostrated that AA had some improvement on LDinduced NAFLD, and its mechanism may be related to SREBP1 and AMPK pathway.