四川大学学报(医学版)
四川大學學報(醫學版)
사천대학학보(의학판)
JOURNAL OF SICHUAN UNIVERSITY(MEDICAL SCIENCE EDITION)
2009年
6期
1075-1077,1090
,共4页
杨孟昌%陈玉培%曹德钧%徐茜%李攀
楊孟昌%陳玉培%曹德鈞%徐茜%李攀
양맹창%진옥배%조덕균%서천%리반
乳化异氟醚%心肌%原代培养%缺氧%复氧
乳化異氟醚%心肌%原代培養%缺氧%複氧
유화이불미%심기%원대배양%결양%복양
Emulsified isoflurane%Cardiac myocyte%Primary culture%Hypoxia%Reoxygenation
目的 探讨乳化异氟醚(EI)对乳鼠原代培养缺氧/复氧(H/R)损伤心肌细胞保护效应的最适浓度.方法 原代培养乳鼠心肌细胞,建立体外心肌细胞H/R损伤模型,随机分为13组:正常组(N组),缺氧/复氧组(H/R组),脂肪乳组(F组),按0.28 mmol/L EI的1、2、3、4、5、6、7、8、9、10倍分别分成EI_1~ EI_(10)组.各组取细胞培养上清液测定乳酸脱氢酶(LDH)活性和心肌肌钙蛋白I(cTnI)含量,细胞匀浆后测定心肌细胞超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.结果 与N组比较,各组的LDH、MDA、cTnI均升高(P<0.05),SOD下降(P<0.05).与H/R组比较,EI各组的LDH、MDA、cTnI均降低(P<0.05),SOD升高(P<0.05).与EI_6组比较,EI其余各组的LDH、MDA、cTnI均升高(P<0.05),SOD下降(P<0.05).随着EI浓度(倍数递增)的增加,EI1~EI6组的LDH、MDA、cTnI逐渐下降,SOD逐渐升高(P<0.05),EI_7~EI_(10)组的LDH、MDA、cTnI逐渐升高,SOD逐渐下降(P<0.05).结论 EI对乳鼠离体心肌细胞H/R损伤具有保护作用,其最佳心肌保护效应浓度为1.68 mmol/L,其机制可能与其抗氧化作用有关.
目的 探討乳化異氟醚(EI)對乳鼠原代培養缺氧/複氧(H/R)損傷心肌細胞保護效應的最適濃度.方法 原代培養乳鼠心肌細胞,建立體外心肌細胞H/R損傷模型,隨機分為13組:正常組(N組),缺氧/複氧組(H/R組),脂肪乳組(F組),按0.28 mmol/L EI的1、2、3、4、5、6、7、8、9、10倍分彆分成EI_1~ EI_(10)組.各組取細胞培養上清液測定乳痠脫氫酶(LDH)活性和心肌肌鈣蛋白I(cTnI)含量,細胞勻漿後測定心肌細胞超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.結果 與N組比較,各組的LDH、MDA、cTnI均升高(P<0.05),SOD下降(P<0.05).與H/R組比較,EI各組的LDH、MDA、cTnI均降低(P<0.05),SOD升高(P<0.05).與EI_6組比較,EI其餘各組的LDH、MDA、cTnI均升高(P<0.05),SOD下降(P<0.05).隨著EI濃度(倍數遞增)的增加,EI1~EI6組的LDH、MDA、cTnI逐漸下降,SOD逐漸升高(P<0.05),EI_7~EI_(10)組的LDH、MDA、cTnI逐漸升高,SOD逐漸下降(P<0.05).結論 EI對乳鼠離體心肌細胞H/R損傷具有保護作用,其最佳心肌保護效應濃度為1.68 mmol/L,其機製可能與其抗氧化作用有關.
목적 탐토유화이불미(EI)대유서원대배양결양/복양(H/R)손상심기세포보호효응적최괄농도.방법 원대배양유서심기세포,건입체외심기세포H/R손상모형,수궤분위13조:정상조(N조),결양/복양조(H/R조),지방유조(F조),안0.28 mmol/L EI적1、2、3、4、5、6、7、8、9、10배분별분성EI_1~ EI_(10)조.각조취세포배양상청액측정유산탈경매(LDH)활성화심기기개단백I(cTnI)함량,세포균장후측정심기세포초양화물기화매(SOD)활성화병이철(MDA)함량.결과 여N조비교,각조적LDH、MDA、cTnI균승고(P<0.05),SOD하강(P<0.05).여H/R조비교,EI각조적LDH、MDA、cTnI균강저(P<0.05),SOD승고(P<0.05).여EI_6조비교,EI기여각조적LDH、MDA、cTnI균승고(P<0.05),SOD하강(P<0.05).수착EI농도(배수체증)적증가,EI1~EI6조적LDH、MDA、cTnI축점하강,SOD축점승고(P<0.05),EI_7~EI_(10)조적LDH、MDA、cTnI축점승고,SOD축점하강(P<0.05).결론 EI대유서리체심기세포H/R손상구유보호작용,기최가심기보호효응농도위1.68 mmol/L,기궤제가능여기항양화작용유관.
Objective To optimize the concentration of emulsified isoflurane (El) for the protective effect on primary cultured neonatal rat hypoxia/reoxygenation (H/R) cardiac myocytes. Methods To prepare the H/R injury model on the basis of in-vitro neonatal rat cardiac myocytes culture and divide them into 13 groups at random, namely, normal control group (N group), H/R group, H/R+fat emulsion group (F group) , the one, two, three, four, five, six, seven, eight, nine and ten times of 0. 28 mmol/L El designated as EI1-EI10 group. The supernatants of cell culture from each group were detected for lactate dehydrogenase (LDH) activity and the level of cardiac troponin-I (cTnl). The cellular homogenates of each group were prepared for the detection of superoxide dismutase (SOD) and malondialdehyde (MDA). Inverted microscope was applied to observe the characteristics of cardiac myocytes growth and changes of its forms. Results Compared to N group, the LDH. MDA and cTnl of others all increased (P<0. 05) and SOD decreased (P<0. 05). Compared to H/R group, LDH, MDA and cTnl of each El dose group decreased significantly (P<0. 05), but SOD increased (P<0. 05). Compared to EL. group, the LDH, MDA and cTnl in the other groups of El increased (P<0. 05) and the SOD decreased (P<0. 05). As the El concentration (increasing by multiple) increased, the LDH, MDA and cTnl in the El1 to EI6 group decreased gradually and SOD gradually increased (P<0. 05), the LDH, MDA and cTnl in the EL to EI10 group increased gradually and SOD gradually decreased (P<0. 05). Conclusion El has the protective effect on the neonatal rat cardiac myocytes with H/R injury, the optimal concentration for the protective effect on cardiac myocytes is 1. 68 mmol/L, and its mechanism may be associated with its anti-oxidation effect.