Objective: To observe the effect of electroacupuncture (EA) stimulation (EAS) of back-shu acupoints on expression of tumor necrosis factor-alpha (TNF-alpha) 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 = 1), 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 8 weeks. EAS was applied to bilateral "Pishu" (BL 20), "Geshu" (BL 17) and "Shenshu" (BL 23) for 20 min, once daily for 4 weeks. Rats of the medication group were treated by 1% Dongbao Gantai suspension (0.28 g/kg, 20 mL/kg) once daily for 4 weeks. 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-alpha was 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-alpha expression, FFA and MDA contents (P < 0.01), and marked down-regulation of SOD activity (P < 0.01). Following 4 weeks' 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-alpha expression 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-alpha expression (P > 0.05).
Conclusion: EA intervention can improve liver fatty degeneration, inhibit high fat induced up-regulation of hepatic TNF-a expression, 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.