Objective To explore the protective effect of electroacupuncture(EA) on hepatic ischemia-reperfusion injury(HIRI) and the expression of high mobility group protein 1(HMGB1) in liver tissues in rats. Methods A total of 40 male SD rats were randomly divided into 4 groups

namely sham control

HIRI model

"Ganshu"(BL18)-"Yanglingquan"(GB34) and non-acupoint group

with 10 rats in each group. The HIRI model was induced by blocking the arteries

veins and bile ducts supplying the middle and left lobes of the liver for 1 h

and reperfusion for 4 h to induce an area of about 70% HIRI. EA was applied to bila-teral BL18 and GB34

or non-acupoints about 6—8 mm to the bilateral BL18 for 30 min before modeling. Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) levels were measured by using an automatic biochemical analyzer. Serum tumor necrosis factor-α(TNF-α)

interleukin-6(IL-6) and HMGB1 levels were assayed by ELISA. Hematoxylin-eosin(H.E.) staining was used to observe histopathological changes of the liver tissue by using tissue injury scaling(0-3 scores). The expression of HMGB1 protein in liver tissues was detected by immunohistochemical staining

Western blot and PCR

separately. Results Following modeling and compared with the sham group

the levels of serum ALT

AST

TNF-α

IL-6

and HMGB1 contents

the number of HMGB1 immunoreaction(IR)-positive cells

and HMGB1 protein and mRNA were significantly increased(P<0.01). After the treatment

the contents of serum ALT

AST

TNF-α

IL-6

and HMGB1

liver HMGB1 IR-positive cells

protein and mRNA were considerably down-regulated in the BL18-GB34 group(P<0.05)

rather than in the non-acupoint group(P>0.05) in contrast to the model group. H.E. stain showed a higher liver injury score in the model group than in the sham group(P<0.01)

and a lower liver injury score in the BL18-GB34 group(not the non-acupoint group) relevant to the model group(P<0.05). Conclusion EA of BL18 and GB34 points has a protective effect on ischemic liver injury in rats with HIRI

which may be associated with its functions in inhibiting the migration and release of HMGB1 from the nucleus to the cytoplasm and in down-regulating the expression of inflammatory factors.