安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
9期
1279-1282,1283
,共5页
陈菁菁%顾尔伟%鲁显福%张雷%刘训芹%程岑
陳菁菁%顧爾偉%魯顯福%張雷%劉訓芹%程岑
진정정%고이위%로현복%장뢰%류훈근%정잠
辛二酰苯胺异羟肟酸%2型糖尿病%舒芬太尼
辛二酰苯胺異羥肟痠%2型糖尿病%舒芬太尼
신이선분알이간우산%2형당뇨병%서분태니
suberoylanilide hydroxamic acid%type 2 diabetes mellitus%sufentanil
目的探讨组蛋白去乙酰酶抑制剂辛二酰苯胺异羟肟酸(SAHA)对2型糖尿病(T2DM)阻碍舒芬太尼后处理心肌保护效应的影响。方法应用SPF级雄性SD大鼠建立糖尿病(DM)和非糖尿病(NDM)模型,各自随机分为6组:假手术组(S组)、缺血再灌注组(I/R组)、舒芬太尼后处理组( SP组)、SAHA加舒芬太尼后处理组( SASP组)、二甲基亚砜加舒芬太尼后处理组( DSSP 组)以及 SAHA 组( SA组)。测定血浆心肌肌钙蛋白I( cTnI)浓度并计算梗死区和缺血危险区之比( IS/AAR )。结果与 NDM-I/R 组相比, NDM-SP、NDM-SASP以及NDM-DSSP组的IS/AAR以及血浆cTnI浓度均下降(P<0.05);与DM-I/R组比较,DM-SP组、DM-DSSP组及DM-SA组IS/AAR和血浆cTnI差异无统计学意义( P>0.05),但 DM-SASP组 IS/AAR以及血浆 cTnI浓度下降(P<0.05)。结论 SAHA可以逆转被T2DM阻碍的舒芬太尼后处理心肌保护效应,推测T2DM阻碍舒芬太尼后处理心肌保护的机制可能与组蛋白乙酰化/去乙酰化有关。
目的探討組蛋白去乙酰酶抑製劑辛二酰苯胺異羥肟痠(SAHA)對2型糖尿病(T2DM)阻礙舒芬太尼後處理心肌保護效應的影響。方法應用SPF級雄性SD大鼠建立糖尿病(DM)和非糖尿病(NDM)模型,各自隨機分為6組:假手術組(S組)、缺血再灌註組(I/R組)、舒芬太尼後處理組( SP組)、SAHA加舒芬太尼後處理組( SASP組)、二甲基亞砜加舒芬太尼後處理組( DSSP 組)以及 SAHA 組( SA組)。測定血漿心肌肌鈣蛋白I( cTnI)濃度併計算梗死區和缺血危險區之比( IS/AAR )。結果與 NDM-I/R 組相比, NDM-SP、NDM-SASP以及NDM-DSSP組的IS/AAR以及血漿cTnI濃度均下降(P<0.05);與DM-I/R組比較,DM-SP組、DM-DSSP組及DM-SA組IS/AAR和血漿cTnI差異無統計學意義( P>0.05),但 DM-SASP組 IS/AAR以及血漿 cTnI濃度下降(P<0.05)。結論 SAHA可以逆轉被T2DM阻礙的舒芬太尼後處理心肌保護效應,推測T2DM阻礙舒芬太尼後處理心肌保護的機製可能與組蛋白乙酰化/去乙酰化有關。
목적탐토조단백거을선매억제제신이선분알이간우산(SAHA)대2형당뇨병(T2DM)조애서분태니후처리심기보호효응적영향。방법응용SPF급웅성SD대서건립당뇨병(DM)화비당뇨병(NDM)모형,각자수궤분위6조:가수술조(S조)、결혈재관주조(I/R조)、서분태니후처리조( SP조)、SAHA가서분태니후처리조( SASP조)、이갑기아풍가서분태니후처리조( DSSP 조)이급 SAHA 조( SA조)。측정혈장심기기개단백I( cTnI)농도병계산경사구화결혈위험구지비( IS/AAR )。결과여 NDM-I/R 조상비, NDM-SP、NDM-SASP이급NDM-DSSP조적IS/AAR이급혈장cTnI농도균하강(P<0.05);여DM-I/R조비교,DM-SP조、DM-DSSP조급DM-SA조IS/AAR화혈장cTnI차이무통계학의의( P>0.05),단 DM-SASP조 IS/AAR이급혈장 cTnI농도하강(P<0.05)。결론 SAHA가이역전피T2DM조애적서분태니후처리심기보호효응,추측T2DM조애서분태니후처리심기보호적궤제가능여조단백을선화/거을선화유관。
Objective To investigate the effects of suberoylanilide hydroxamic acid( SAHA, as a histone deacety-lase inhibitor) in the attenuation of cardioprotective effect by sufentanil postconditioning in type 2 diabetes mellitus ( T2DM) rats. Methods Male SD rats of SPF grade were included to establish diabetic as well as non-diabetic rat models. Both types were randomly divided into 6 groups respectively:sham-operated group ( Group S);ischemia-reperfusion group ( Group I/R); sufentanil postconditioning group ( Group SP); SAHA plus sufentanil postcondi-tioning group ( Group SASP);DMSO plus sufentanil postconditioning group ( Group DSSP);SAHA group ( Group SA) . Both measurement of plasma concentration of cardiac troponin I ( cTnI) and calculation of IS/AAR were ac-complished. Results In group NDM-SP, NDM-SASP and NDM-DSSP, the IS/ARR and plasma concentrations of cTnI significantly decreased compared with group NDM-I/R ( P<0.05 ) . There was no statistical significance a-mong groups of DM-I/R, DM-SP, DM-DSSP and DM-SA in the IS/ARR and plasma concentrations of cTnI ( P>0.05 ) , while adding the intervention of sufentanil postconditioning to group DM-SP brought down indexes men-tioned above dramatically ( P <0.05 ) . Conclusion In the case that SAHA could restore the cardioprotective effects of sufentanil postconditioning which were once blocked due to T2DM, there might exist links between the mechanism of this obstruction and modification of histone acetylation/deacetylation.