Effect of electroacupuncture at Zusanli on liver injury during early stage after burn in rats / 中华麻醉学杂志

ABSTRACT

Objective To. investigate the effect of electroacupuncture at acupoint Zusanli (ST36) on the liver injury during the early stage after bum in rats. Methods Forty adult male SD rats weighing 220-250 g were randomly divided into 5 groups ( n = 8 each) group sham operation (group Ⅰ ) ; group burn (group Ⅱ ) ; group acupoint at Zusanli (ST36) (group Ⅲ ); group non-acupoint stimulation (group Ⅳ ) and group ST36 + alphabungarotoxin (alpha7 nicotinic acetylcholine receptor antagonist) (group Ⅴ ). Rats were subjected to 3rd degree burn covering 30% of the total body surface area. Rats were resuscitated with lactataed Ringer's solution according to Parkland formula (4 ml/kg per 1% body surface area) immediately after burn. Bilateral acupoints Zusanli were stimulated with constant voltage (3 V, 3 Hz,2ms) for 20 min 3 times a day for 2 days starting immediately after resuscitation in H and V groups. In group V alpha-bungarotoxin 1.0 μg/kg was administered iv immediately after fluid resuscitation before acupuncture. In group Ⅳ same electric stimulation was performed at a point 0.5 cm lateral to Zusanli. The animals were sacrificed at 48 h after burn. The content and expression of high mobility group box 1 (HMGB1) protein in liver were measured. Liver specimens were obtained for microscopic examination (with light and electronic microscope). Results Compared with group Ⅰ , hepatic HMGB1 protein level significantly increased in Ⅱ and Ⅳ groups. There were significant ultrastructural changes in the liver in burn rats in group Ⅱ and group Ⅳ. Electric stimulation of ST36 significantly attenuated the histologic changes in the liver and decreased the hepatic HMGB1 protein level in group Ⅲ . Pretreatment with specific alpha.7 nicotinie acetylcholine receptor antagonist alpha-bungarotoxin reversed the beneficial effect of electroacupuncture at Zusanli. Conclusion Electric stimulation of acupoint ST36 can ameliorate liver injury during the early stage of burn by activating alpha7 nicotinic acetylcholine receptor-mediated pathways for anti-inflammation.