The Protective Effect Of Electroacupuncture Against CPB- Induced ALI

Objective: Our previous study revealed that high mobility group box1(HMGB1),the key initiate factor of acute lung injury(ALI),released after lung ischemia reperfusion injury(IRI)during cardiopulmonary bypass(CPB).Cholinergic anti-inflammatory pathway(CAP)was proved to inhibite the release of HMGB1 during IRI.Numerous studies have shown that electroacupuncture(EA)can inhibit the inflammation of the body by regulating the autonomic nervous system.In this study,we assessed the effect of EA pretreatment on the expression of ?7 nicotinic acetylcholine receptors(?7n ACh R),using CPB in rats.Further,we investigated the role of high mobility group box 1(HMGB1)in lung-protection mediated by the a7 n ACh R and EA.Methods: This study employed EA and a rat model of CPB to determine whether EA was associated with CPB-induced lung injury.Rats were treated with EA at “Zusanli(ST36)”and “Feishu(BL13)” acupoints for 5 days before being subjected to CPB.Two hours post-CPB,samples of blood,bronchoalveolar lavage fluid(BALF)and lung tissues were processed for investigations.The ?7n ACh R agonist PHA-543613 and the antagonist ?-bungarotoxin(?-BGT)were used to investigate the role of the a7 n ACh R in mediating lung-protective effects.The roles of the ?7n ACh R and HMGB1 release in the protection of lung were further tested in macrophages exposed to oxygen and glucose deprivation(OGD).Results: Our results showed that the expression of ?7n ACh R in lung tissue was significantly decreased after CPB.EA pretreatment prevented the reduction in the expression of ?7n ACh R,EA pretreatment reduced lung edema,inhibited inflammatory cytokines release in serum and lung as well as protein concentrations in BALF and HMGB1 release following CPB,and the beneficial effects were attenuated by ?-BGT.Furthermore,OGD in macrophages triggered HMGB1 release into the culture medium,and this effect was efficiently suppressed by PHA-543,613.Pretreatment with a-BGT reversed the inhibitory effect of PHA-543,613 on HMGB1 release.Conclusion: Our study demonstrates that EA pretreatment plays a protective role in CPB-induced ALI,and inhibits HMGB1 release through ?7n ACh R activation in rats.