中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
10期
2477-2480
,共4页
李鑫%刘一丹%吴建江%王江%郑宏
李鑫%劉一丹%吳建江%王江%鄭宏
리흠%류일단%오건강%왕강%정굉
七氟烷%糖原合成酶激酶-3β%再灌注损伤%预处理%后处理
七氟烷%糖原閤成酶激酶-3β%再灌註損傷%預處理%後處理
칠불완%당원합성매격매-3β%재관주손상%예처리%후처리
Sevoflurane%Glycogen synthase kinase-3β%Reperfusion injury%Preconditioning%Postconditioning
目的 观察七氟烷预处理联合后处理对高糖培养原代心肌细胞缺氧/复氧损伤的保护作用,并探讨糖原合成酶激酶-3β(GSK-3β)在高糖弱化七氟烷心肌保护效应中的作用.方法 健康新生1～3 d SD大鼠,于无菌条件下取出心脏.随机分为2大组,共12小组,正常组采用低糖(葡萄糖浓度:5.56 mmol/L) DMEM培养液进行培养.高糖组采用高糖(葡萄糖浓度:25 mmol/L)DMEM培养液进行培养.(1)对照组(NC、HC组);(2)缺氧/复氧组(NH/R、HH/R组);(3)七氟烷后处理组(NS-Post、HS-Post组);(4)七氟烷预处理联合后处理组(NS-Pre+ S-Post、HS-Pre+ S-Psot组);(5)SB216763组(NSB、HSB组);(6)二甲基亚砜组(N-DMSO、H-DMSO组).复氧结束后对各组细胞存活率、细胞凋亡率、培养液LDH活性、磷酸化GSK-3β(P-GSK-3β)蛋白表达水平进行检测.结果 NH/R、NS-Post、NS-Pre+ S-Post组细胞存活率分别为(52.4±3.4)％、(61.1±4.5)％、(71.2±2.8)％,与NH/R组比较,NS-Post、NS-Pre+ S-Post组细胞存活率升高,HH/R、HS-Post、HS-Pre+S-Post组细胞存活率分别为(48.2±5.1)％、(50.8±4.9)％、(48.5±2.8)％.细胞凋亡率降低,培养液LDH活性降低,P-GSK-3β蛋白表达水平上调(P＜0.05).与HH/R组比较,HS-Post、HS-Pre+S-Post组各项指标均未见明显差异(P＞0.05).结论 七氟烷预处理联合后处理亦无法对高糖培养心肌细胞缺氧/复氧损伤发挥保护作用,GSK-3β参与了高糖所致七氟烷心肌保护作用弱化的过程.
目的 觀察七氟烷預處理聯閤後處理對高糖培養原代心肌細胞缺氧/複氧損傷的保護作用,併探討糖原閤成酶激酶-3β(GSK-3β)在高糖弱化七氟烷心肌保護效應中的作用.方法 健康新生1～3 d SD大鼠,于無菌條件下取齣心髒.隨機分為2大組,共12小組,正常組採用低糖(葡萄糖濃度:5.56 mmol/L) DMEM培養液進行培養.高糖組採用高糖(葡萄糖濃度:25 mmol/L)DMEM培養液進行培養.(1)對照組(NC、HC組);(2)缺氧/複氧組(NH/R、HH/R組);(3)七氟烷後處理組(NS-Post、HS-Post組);(4)七氟烷預處理聯閤後處理組(NS-Pre+ S-Post、HS-Pre+ S-Psot組);(5)SB216763組(NSB、HSB組);(6)二甲基亞砜組(N-DMSO、H-DMSO組).複氧結束後對各組細胞存活率、細胞凋亡率、培養液LDH活性、燐痠化GSK-3β(P-GSK-3β)蛋白錶達水平進行檢測.結果 NH/R、NS-Post、NS-Pre+ S-Post組細胞存活率分彆為(52.4±3.4)％、(61.1±4.5)％、(71.2±2.8)％,與NH/R組比較,NS-Post、NS-Pre+ S-Post組細胞存活率升高,HH/R、HS-Post、HS-Pre+S-Post組細胞存活率分彆為(48.2±5.1)％、(50.8±4.9)％、(48.5±2.8)％.細胞凋亡率降低,培養液LDH活性降低,P-GSK-3β蛋白錶達水平上調(P＜0.05).與HH/R組比較,HS-Post、HS-Pre+S-Post組各項指標均未見明顯差異(P＞0.05).結論 七氟烷預處理聯閤後處理亦無法對高糖培養心肌細胞缺氧/複氧損傷髮揮保護作用,GSK-3β參與瞭高糖所緻七氟烷心肌保護作用弱化的過程.
목적 관찰칠불완예처리연합후처리대고당배양원대심기세포결양/복양손상적보호작용,병탐토당원합성매격매-3β(GSK-3β)재고당약화칠불완심기보호효응중적작용.방법 건강신생1～3 d SD대서,우무균조건하취출심장.수궤분위2대조,공12소조,정상조채용저당(포도당농도:5.56 mmol/L) DMEM배양액진행배양.고당조채용고당(포도당농도:25 mmol/L)DMEM배양액진행배양.(1)대조조(NC、HC조);(2)결양/복양조(NH/R、HH/R조);(3)칠불완후처리조(NS-Post、HS-Post조);(4)칠불완예처리연합후처리조(NS-Pre+ S-Post、HS-Pre+ S-Psot조);(5)SB216763조(NSB、HSB조);(6)이갑기아풍조(N-DMSO、H-DMSO조).복양결속후대각조세포존활솔、세포조망솔、배양액LDH활성、린산화GSK-3β(P-GSK-3β)단백표체수평진행검측.결과 NH/R、NS-Post、NS-Pre+ S-Post조세포존활솔분별위(52.4±3.4)％、(61.1±4.5)％、(71.2±2.8)％,여NH/R조비교,NS-Post、NS-Pre+ S-Post조세포존활솔승고,HH/R、HS-Post、HS-Pre+S-Post조세포존활솔분별위(48.2±5.1)％、(50.8±4.9)％、(48.5±2.8)％.세포조망솔강저,배양액LDH활성강저,P-GSK-3β단백표체수평상조(P＜0.05).여HH/R조비교,HS-Post、HS-Pre+S-Post조각항지표균미견명현차이(P＞0.05).결론 칠불완예처리연합후처리역무법대고당배양심기세포결양/복양손상발휘보호작용,GSK-3β삼여료고당소치칠불완심기보호작용약화적과정.
Objective To evaluate the effecof sevoflurane pre-and post-conditioning on hypoxia/reoxgenation-induced injury of neonatal racardiomyocytecultured in high-glucose culture medium and the role of glycogen synthase kinase-3β.MethodPrimary cultured neonatal ra(1-3 d aftebirth) cardiomyocytewere randomly divided into 12 groups: Normal groupuse low-glucose (concentration,5.56 mmol/L) DMEM medium, hyperglycemigroupuse high-glucose (concentration, 25 mmol/L)DMEM medium.Control group (group NC/HC);hypoxia/reoxgenation group (group NH/R/HH/R);sevoflurane postconditioning group (group NS-Post/HS-Post);sevoflurane pre-and post-conditioning group (group NS-Pre + S-Post/HS-Pre + S-Post);SB216763 group (group NSB/HSB);Dimethyl sulfoxide group (group N-DMSO/H-DMSO).Cell survival rate, apoptotirate, the LDH activity and the levelof phosphor-GSK-3β were measured athe end of the experiment.ResultNH/R,HS-Post, HS-Pre + S-Posgroup were (52.4 ± 3.4) ％, (61.1 ± 4.5) ％, (71.2 ± 2.8) ％, respectively.HS-Posgroup、HS-Pre + S-Posgroup reduced the apoptotirate compared with group NH/R.However, HH/R, HS-Post, HS-Pre +S-Posgroup were (48.2 5.1)％, (50.8 ±4.9)％,(48.5 ± 2.8) ％, respectively.HS-Posgroup, HS-Pre + S-Posgroup didn' reduce the apoptotirate compared with group NH/R.Conclusion Cardioprotection induced by sevoflurane iabolished by hyperglycemia.GSK-3β may be involved with above processes.
