临床外科杂志
臨床外科雜誌
림상외과잡지
JOURNAL OF CLINICAL SURGERY
2014年
8期
603-605
,共3页
盐酸戊乙奎醚%心肌细胞%脂多糖%核因子-κB
鹽痠戊乙奎醚%心肌細胞%脂多糖%覈因子-κB
염산무을규미%심기세포%지다당%핵인자-κB
penehyclidine hydrochloride%cardiomyocyte%lipopolysaccharide%NF-κB
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。
目的：探討鹽痠戊乙奎醚（penehyclidine hydrochloride，PHC）對脂多糖（LPS）誘導新生乳鼠心肌細胞損傷的影響及機製。方法體外培養1 d 齡新生乳鼠心肌細胞。隨即分為四組：對照組、LPS 組、低劑量 PHC 預處理組和高劑量 PHC 預處理組。檢測各組心肌酶和肌鈣蛋白水平、細胞存活率。免疫印跡法檢測胞覈 NF-κB p65亞單位及胞漿 NF-κB 抑製蛋白 IκB-α燐痠化水平。結果與對照組相比，LPS 組心肌酶和肌鈣蛋白水平明顯上調，而細胞存活率明顯下降；在不同劑量 PHC 預處理組，以上效應均被抑製。LPS 組胞覈 NF-κB p65亞單位錶達及胞漿 NF-κB 抑製蛋白IκB-α燐痠化水平均上調；而 PHC 預處理組胞覈 NF-κB p65亞單位錶達及胞漿 NF-κB 抑製蛋白IκB-α燐痠化水平均下調。結論PHC 可抑製 LPS 誘導的乳鼠心肌細胞損傷，其機製可能與下調NF-κB 活化有關。
목적：탐토염산무을규미（penehyclidine hydrochloride，PHC）대지다당（LPS）유도신생유서심기세포손상적영향급궤제。방법체외배양1 d 령신생유서심기세포。수즉분위사조：대조조、LPS 조、저제량 PHC 예처리조화고제량 PHC 예처리조。검측각조심기매화기개단백수평、세포존활솔。면역인적법검측포핵 NF-κB p65아단위급포장 NF-κB 억제단백 IκB-α린산화수평。결과여대조조상비，LPS 조심기매화기개단백수평명현상조，이세포존활솔명현하강；재불동제량 PHC 예처리조，이상효응균피억제。LPS 조포핵 NF-κB p65아단위표체급포장 NF-κB 억제단백IκB-α린산화수평균상조；이 PHC 예처리조포핵 NF-κB p65아단위표체급포장 NF-κB 억제단백IκB-α린산화수평균하조。결론PHC 가억제 LPS 유도적유서심기세포손상，기궤제가능여하조NF-κB 활화유관。
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.
