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目的：探讨盐酸戊乙奎醚（penehyclidine hydrochloride，PHC）对脂多糖（LPS）诱导新生乳鼠心肌细胞损伤的影响及机制。方法体外培养1 d 龄新生乳鼠心肌细胞。随即分为四组：对照组、LPS 组、低剂量 PHC 预处理组和高剂量 PHC 预处理组。检测各组心肌酶和肌钙蛋白水平、细胞存活率。免疫印迹法检测胞核 NF-κB p65亚单位及胞浆 NF-κB 抑制蛋白 IκB-α磷酸化水平。结果与对照组相比，LPS 组心肌酶和肌钙蛋白水平明显上调，而细胞存活率明显下降；在不同剂量 PHC 预处理组，以上效应均被抑制。LPS 组胞核 NF-κB p65亚单位表达及胞浆 NF-κB 抑制蛋白IκB-α磷酸化水平均上调；而 PHC 预处理组胞核 NF-κB p65亚单位表达及胞浆 NF-κB 抑制蛋白IκB-α磷酸化水平均下调。结论PHC 可抑制 LPS 诱导的乳鼠心肌细胞损伤，其机制可能与下调NF-κB 活化有关。“,”Objective To observe the effects of penehyclidine hydrochloride(PHC)on lipopo-lysaccharide-induced neonatal cardiomyocyte damage.Methods After the primary cardiomyocytes culture of neonatal rat on postnatal day 1,the myocytes were randomly divided into 4 groups:the control group,the lipopolysaccharide(LPS)group,the low dosage PHC pretreatment group and high dosage PHC pretreatment group.Activities of myocardial enzymes and cardiac troponin and cell survival rate were measured.Expres-sion of NF-Κb(p65)and IκB-α(NF-κB inhibitor)phosphorylation were assessed using Western blot.Re-sults Compared with the control group,activities of myocardial enzymes and cardiac troponin in the LPS group were elevated but the survival rate were down-regulated.All these effects were reversed in the PHC pretreatment group.Results of Western blot showed that phosphorylation of IκB-αand p65 expression were up-regulated in the LPS group.In the PHC pretreatment group,phosphorylation of IκB-αand p65 expres-sion were down-regulated.Conclusion Penehyclidine hydrochloride can inhibit lipopolysaccharide-in-duced neonatal cardiomyocyte damage and the down-regulation of NF-κB activity might be involved.