中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2012年
5期
589-592
,共4页
异氟醚/药理学%肿瘤坏死因子α/代谢%肾/病理学%缺血预处理%再灌注损伤%大鼠
異氟醚/藥理學%腫瘤壞死因子α/代謝%腎/病理學%缺血預處理%再灌註損傷%大鼠
이불미/약이학%종류배사인자α/대사%신/병이학%결혈예처리%재관주손상%대서
Isoflurane/pharmacology%Tumor necrosis factor-alpha/metabolism%Kidney/pathol-gy%lschemic preconditioning%Reperfusion injury%Rats
目的 观察异氟醚预处理对大鼠肾缺血再灌注(ischemia-reperfusion,I/R)损伤的影响,并探讨肿瘤坏死因子-α( TNF-α)在其中的作用.方法 健康成年雄性SD大鼠36只,随机分成假手术组(S组),缺血再灌注组(L/R组)和异氟醚预处理组(Iso+ I/R组),每组各12只.S组进腹后仅分离韧带不阻断血流；I/R组行肾脏缺血45 min,再灌注2h；Iso+I/R组吸入1.5％ (1MAC)异氟醚30 min,停止吸人10 min后行I/R.在再灌注2h后测定血清尿素氮(BUN)和肌酐(Cr)的含量,采用双抗体夹心酶联免疫吸附试验(ELISA法)测定肾组织中TNF-α的浓度,同时取肾组织进行HE染色观察病理学改变.结果 (1)与S组比较,I/R组和Iso+I/R组血清BUN和Cr表达水平、肾组织中TNF-α浓度均升高[BUN:( 17.69±0.99) mmol/L vs(8.37±1.12)mmol/L,t=-23.55,P＜0.01;(12.26±1.11)mmol/L vs (8.37±1.12)mmol/L,t=- 19.09,P ＜0.01;Cr:(103.22±13.42)μmol/L vs(71.48±8.59) μmol/L,t=-21.45,P＜0.01;(86.51±11.49)μmol/Lvs(71.48±8.59) μmol/L,t=-9.87,P＜0.01;TNF-α:(0.51±0.07)ng/ml vs(0.43±0.00)ng/ml,t=-5.79,P＜0.01;(0.47±0.03)ng/mlvs(0.43±0.00)ng/ml,t=-8.86,P ＜0.01].(2)Iso +I/R组血清BUN和Cr表达水平、肾组织中TNF-α浓度的升高幅度均小于I/R组[BUN:( 12.26±1.11)mmol/L vs( 17.69±0.99)mmol/L,t=15.67,P＜0.01;Cr:(86.51±11.49) μmol/L vs(103.22±13.42) μmol/L,t=6.68,P＜0.01;TNF-α:(0.47±0.03)ng/ml vs (0.51±0.07)ng/ml,t =2.61,P ＜0.05].(3)I/R组、Iso+ I/R组肾小管评分较S组升高[(17.26±1.45)vs(0.00±0.00),t=-72.38,P＜0.01；(12.69±1.83)vs(0.00±0.00),t=- 39.53,P＜0.01].Iso+I/R组肾小管评分较I/R组下降[(12.69±1.83) vs (17.26±1.45),t=19.87,P＜0.01].结论 1.5％异氟醚预处理30min可减轻大鼠肾缺血再灌注损伤,其部分机制可能与下调肾组织中TNF-α水平有关.
目的 觀察異氟醚預處理對大鼠腎缺血再灌註(ischemia-reperfusion,I/R)損傷的影響,併探討腫瘤壞死因子-α( TNF-α)在其中的作用.方法 健康成年雄性SD大鼠36隻,隨機分成假手術組(S組),缺血再灌註組(L/R組)和異氟醚預處理組(Iso+ I/R組),每組各12隻.S組進腹後僅分離韌帶不阻斷血流；I/R組行腎髒缺血45 min,再灌註2h；Iso+I/R組吸入1.5％ (1MAC)異氟醚30 min,停止吸人10 min後行I/R.在再灌註2h後測定血清尿素氮(BUN)和肌酐(Cr)的含量,採用雙抗體夾心酶聯免疫吸附試驗(ELISA法)測定腎組織中TNF-α的濃度,同時取腎組織進行HE染色觀察病理學改變.結果 (1)與S組比較,I/R組和Iso+I/R組血清BUN和Cr錶達水平、腎組織中TNF-α濃度均升高[BUN:( 17.69±0.99) mmol/L vs(8.37±1.12)mmol/L,t=-23.55,P＜0.01;(12.26±1.11)mmol/L vs (8.37±1.12)mmol/L,t=- 19.09,P ＜0.01;Cr:(103.22±13.42)μmol/L vs(71.48±8.59) μmol/L,t=-21.45,P＜0.01;(86.51±11.49)μmol/Lvs(71.48±8.59) μmol/L,t=-9.87,P＜0.01;TNF-α:(0.51±0.07)ng/ml vs(0.43±0.00)ng/ml,t=-5.79,P＜0.01;(0.47±0.03)ng/mlvs(0.43±0.00)ng/ml,t=-8.86,P ＜0.01].(2)Iso +I/R組血清BUN和Cr錶達水平、腎組織中TNF-α濃度的升高幅度均小于I/R組[BUN:( 12.26±1.11)mmol/L vs( 17.69±0.99)mmol/L,t=15.67,P＜0.01;Cr:(86.51±11.49) μmol/L vs(103.22±13.42) μmol/L,t=6.68,P＜0.01;TNF-α:(0.47±0.03)ng/ml vs (0.51±0.07)ng/ml,t =2.61,P ＜0.05].(3)I/R組、Iso+ I/R組腎小管評分較S組升高[(17.26±1.45)vs(0.00±0.00),t=-72.38,P＜0.01；(12.69±1.83)vs(0.00±0.00),t=- 39.53,P＜0.01].Iso+I/R組腎小管評分較I/R組下降[(12.69±1.83) vs (17.26±1.45),t=19.87,P＜0.01].結論 1.5％異氟醚預處理30min可減輕大鼠腎缺血再灌註損傷,其部分機製可能與下調腎組織中TNF-α水平有關.
목적 관찰이불미예처리대대서신결혈재관주(ischemia-reperfusion,I/R)손상적영향,병탐토종류배사인자-α( TNF-α)재기중적작용.방법 건강성년웅성SD대서36지,수궤분성가수술조(S조),결혈재관주조(L/R조)화이불미예처리조(Iso+ I/R조),매조각12지.S조진복후부분리인대불조단혈류；I/R조행신장결혈45 min,재관주2h；Iso+I/R조흡입1.5％ (1MAC)이불미30 min,정지흡인10 min후행I/R.재재관주2h후측정혈청뇨소담(BUN)화기항(Cr)적함량,채용쌍항체협심매련면역흡부시험(ELISA법)측정신조직중TNF-α적농도,동시취신조직진행HE염색관찰병이학개변.결과 (1)여S조비교,I/R조화Iso+I/R조혈청BUN화Cr표체수평、신조직중TNF-α농도균승고[BUN:( 17.69±0.99) mmol/L vs(8.37±1.12)mmol/L,t=-23.55,P＜0.01;(12.26±1.11)mmol/L vs (8.37±1.12)mmol/L,t=- 19.09,P ＜0.01;Cr:(103.22±13.42)μmol/L vs(71.48±8.59) μmol/L,t=-21.45,P＜0.01;(86.51±11.49)μmol/Lvs(71.48±8.59) μmol/L,t=-9.87,P＜0.01;TNF-α:(0.51±0.07)ng/ml vs(0.43±0.00)ng/ml,t=-5.79,P＜0.01;(0.47±0.03)ng/mlvs(0.43±0.00)ng/ml,t=-8.86,P ＜0.01].(2)Iso +I/R조혈청BUN화Cr표체수평、신조직중TNF-α농도적승고폭도균소우I/R조[BUN:( 12.26±1.11)mmol/L vs( 17.69±0.99)mmol/L,t=15.67,P＜0.01;Cr:(86.51±11.49) μmol/L vs(103.22±13.42) μmol/L,t=6.68,P＜0.01;TNF-α:(0.47±0.03)ng/ml vs (0.51±0.07)ng/ml,t =2.61,P ＜0.05].(3)I/R조、Iso+ I/R조신소관평분교S조승고[(17.26±1.45)vs(0.00±0.00),t=-72.38,P＜0.01；(12.69±1.83)vs(0.00±0.00),t=- 39.53,P＜0.01].Iso+I/R조신소관평분교I/R조하강[(12.69±1.83) vs (17.26±1.45),t=19.87,P＜0.01].결론 1.5％이불미예처리30min가감경대서신결혈재관주손상,기부분궤제가능여하조신조직중TNF-α수평유관.
Objective To investigate the effects of isoflurane preconditioning on renal ischemia reperfusion (I/R) injury in rats and the role of TNF-α plays in the mechanism.Methods Male SD rats were used in the study.The animals were randomly divided into 3 groups ( n =12 each):shame operation group; I/R group; Isoflurane preconditioning group (inhaled 1.5％ isoflurane (1 MAC) for 30 min followed by 10 min washout before I/R).At 2 h reperfusion,blood samples were obtained for urea nitrogen (BUN) concentration and creatinine (Cr) content.The level of TNF-α in renal tissues were determined by enzyme-linked immunosorbent assay (ELISA).Observe the pathological changes in H.E.staining slides under microscope.Results BUN concentration and Cr content and the level of TNF-α in I/R group and isoflurane preconditioning group were significantly higher than in shame operation group[ BUN:( 17.69 ±0.99)mmol/L vs (8.37 ±1.12)mmol/L,t =-23.55,P ＜0.01; ( 12.26 ± 1.11 ) mmol/L vs (8.37 ±1.12 )mmol/L,t =- 19.09,P ＜ 0.01 ;Cr:( 103.22 ± 13.42)μmol/L vs (71.48 ± 8.59) μ mol/L,t =-21.45,P ＜0.01;(86.51 ± 11.49) μmol/L vs (71.48 ±8.59) μmol/L,t =-9.87,P ＜0.01 ;TNF-α:(0.51 ±0.07)ng/ml vs (0.43 ±0.00)ng/ml,t =-5.79,P ＜0.01;(0.47 ±0.03)ng/ml vs (0.43 ±0.00)ng/ml,t =-8.86,P ＜0.01 ].BUN concentration and Cr content and the level of TNF-α in Isoflurane preconditioning group were significantly lower than in I/R group [ BUN:( 12.26 ± 1.1 1 ) mmol/L vs ( 17.69 ± 0.99 ) mmol/L,t =15.67,P ＜ 0.01 ; Cr:( 86.51 ± 11.49) μmol/L vs ( 103.22 ± 13.42 ) μ mol/L,t =6.68,P ＜0.01 ;TNF-α:(0.47 ±0.03) ng/ml vs (0.51 ±0.07) ng/ml,t =2.61,P ＜0.05].Therenal I/R injury which located around kidney tubules was increased in I/R group and isoflurane precondi-tioning group compared to shame operation group [ ( 17.26 ± 1.45 ) vs (0.00 ± 0.00 ),t =- 72.38,P ＜0.01;(12.69±1.83) vs (0.00 ±0.00),t =-39.53,P ＜0.01].The renal I/R injury which located around kidney tubules was decreased in isoflurane preconditioning group compared to I/R group [ ( 12.69 ±1.83) vs (17.26±1.45),t =19.87,P ＜0.01].Conclusions Preconditioning with 1.5％ isoflurane 30 min can protect kidney from I/R injury in rats by regulating the level of TNF-α in renal tissues.
