Objective To observe the effect of electroacupuncture(EA)stimulation(EAS)of back-shu acupoints on expression of tumor necrosis factor-α(TNF-α)and lipid peroxidase reaction in the liver in non-alcoholic fatty liver disease(NAFLD)rats.Methods Wistar rats were randomly divided into normal group(n=11)

model group(n=10)

EAS group(n=10)and medication group(n=10).The NAFLD model was established by feeding the animals with high fat diet for 8weeks.EAS was applied to bilateral"Pishu"(BL 20)

"Geshu"(BL 17)and"Shenshu"(BL 23)for 20 min

once daily for 4weeks.Rats of the medication group were treated by 1% Dongbao Gantai suspension(0.28g/kg

20mL/kg)once daily for 4weeks.Pathological changes of the liver tissue were observed by microscope after H.E.staining.Hepatic free fatty acid(FFA)content was assayed by using an automatic biochemistry analyzer

malondialdehyde(MDA)content and superoxide dismutase(SOD)activity were detected by penthiobarbituric acid colorimetric method and xanthine oxidase colorimetric method

respectively.The expression of liver TNF-αwas detected by immunohistochemistry.Results Compared with the normal group

rats of the model group showed a moderate to severe fatty degeneration of liver cells

significant up-regulation of hepatic TNF-αexpression

FFA and MDA contents(P<0.01)

and marked down-regulation of SOD activity(P<0.01).Following 4weeks' treatment

compared with the model group

liver fatty degeneration was reduced at different degrees in both EAS and medication groups;liver FFA and MDA contents and TNF-αexpression were significantly down-regulated(P<0.01

P<0.05)

and hepatic SOD activity was notably increased(P<0.01

P<0.05)in both EAS and medication groups

suggesting a reduction of hepatic lipid peroxidation.No significant differences between the EAS and medication groups in the liver FFA and MDA contents

SOD activity and TNF-αexpression(P>0.05).Conclusion EA intervention can improve liver fatty degeneration

inhibit high fat induced up-regulation of hepatic TNF-αexpression

FFA and MDA contents and down-regulation of SOD activity in non-alcohol fatty liver model rats

which may contribute to its effect in improving NAFLD.