医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2015年
9期
1161-1164
,共4页
李鑫%冯园园%孙璇璇%李冰
李鑫%馮園園%孫璇璇%李冰
리흠%풍완완%손선선%리빙
替米沙坦%高血压,肾性%心肌重构%钙调神经磷酸酶%β-肌球蛋白重链
替米沙坦%高血壓,腎性%心肌重構%鈣調神經燐痠酶%β-肌毬蛋白重鏈
체미사탄%고혈압,신성%심기중구%개조신경린산매%β-기구단백중련
Telmisartan%Hypertension,renovascular%Myocardial remodeling%Calcium and nerve phosphatase%β-myosin heavy chain
目的：探讨替米沙坦对肾性高血压大鼠心肌重构的影响。方法通过左肾动脉缩窄法建立大鼠肾性高血压心肌肥厚模型,45只雄性斯泼累格?多雷(SD)大鼠随机分为假手术组、模型对照组和替米沙坦组,每组15只。替米沙坦组灌胃替米沙坦10 mg?kg－1?d－1,假手术组、模型对照组灌胃等量纯化水。灌胃8周后,心脏超声诊断仪观察心脏结构和功能,测定血压,计算左心室质量指数,并检测血清中钙调神经磷酸酶(CaN)含量以及心肌β-肌球蛋白重链(β-MHC)mRNA 的表达。结果模型对照组和替米沙坦组左心室射血分数分别为(69.23±1.09)％和(73.77±3.0)％(P<0.05)；缩短分数分别为(30.21±2.02)％和(35.29±0.90)％(P<0.05)；左心室质量指数分别为(2.83±0.14)和(2.32±0.11) mg?g－1(P<0.05)。与模型对照组比较,替米沙坦组外周循环血液中 CaN 以及心肌组织中β-MHC mRNA 的表达均下降(均 P<0.05)。结论替米沙坦可有效逆转由肾性高血压引起的心肌肥厚,并可能通过抑制起始信号 CaN 的活化,作用于下游信号通路,下调心肌蛋白相关基因β-MHC 的表达。
目的：探討替米沙坦對腎性高血壓大鼠心肌重構的影響。方法通過左腎動脈縮窄法建立大鼠腎性高血壓心肌肥厚模型,45隻雄性斯潑纍格?多雷(SD)大鼠隨機分為假手術組、模型對照組和替米沙坦組,每組15隻。替米沙坦組灌胃替米沙坦10 mg?kg－1?d－1,假手術組、模型對照組灌胃等量純化水。灌胃8週後,心髒超聲診斷儀觀察心髒結構和功能,測定血壓,計算左心室質量指數,併檢測血清中鈣調神經燐痠酶(CaN)含量以及心肌β-肌毬蛋白重鏈(β-MHC)mRNA 的錶達。結果模型對照組和替米沙坦組左心室射血分數分彆為(69.23±1.09)％和(73.77±3.0)％(P<0.05)；縮短分數分彆為(30.21±2.02)％和(35.29±0.90)％(P<0.05)；左心室質量指數分彆為(2.83±0.14)和(2.32±0.11) mg?g－1(P<0.05)。與模型對照組比較,替米沙坦組外週循環血液中 CaN 以及心肌組織中β-MHC mRNA 的錶達均下降(均 P<0.05)。結論替米沙坦可有效逆轉由腎性高血壓引起的心肌肥厚,併可能通過抑製起始信號 CaN 的活化,作用于下遊信號通路,下調心肌蛋白相關基因β-MHC 的錶達。
목적：탐토체미사탄대신성고혈압대서심기중구적영향。방법통과좌신동맥축착법건립대서신성고혈압심기비후모형,45지웅성사발루격?다뢰(SD)대서수궤분위가수술조、모형대조조화체미사탄조,매조15지。체미사탄조관위체미사탄10 mg?kg－1?d－1,가수술조、모형대조조관위등량순화수。관위8주후,심장초성진단의관찰심장결구화공능,측정혈압,계산좌심실질량지수,병검측혈청중개조신경린산매(CaN)함량이급심기β-기구단백중련(β-MHC)mRNA 적표체。결과모형대조조화체미사탄조좌심실사혈분수분별위(69.23±1.09)％화(73.77±3.0)％(P<0.05)；축단분수분별위(30.21±2.02)％화(35.29±0.90)％(P<0.05)；좌심실질량지수분별위(2.83±0.14)화(2.32±0.11) mg?g－1(P<0.05)。여모형대조조비교,체미사탄조외주순배혈액중 CaN 이급심기조직중β-MHC mRNA 적표체균하강(균 P<0.05)。결론체미사탄가유효역전유신성고혈압인기적심기비후,병가능통과억제기시신호 CaN 적활화,작용우하유신호통로,하조심기단백상관기인β-MHC 적표체。
Objective To investigate the the molecular mechanism of telmisartan for myocardial remodeling in rats with renovascular hypertention. Methods The renovascular hypertensive myocardial hypertrophy model of rats were established by narrowing the left renal artery.The total of 45 mature male SD rats were divided into sham-operated group(n= 15),model control (n = 15 ) and telmisartan group ( n = 15 ) randomly. The rats in telmisartan group were treated with telmisartan (10 mg?kg-1?d-1 ) while those in the sham-operated and model control were reated with the same amounts of distilled water by intragastrical administration . At 8th week of administration, the myocardial structure and function were detected by ultrasonography.The blood pressure was measured by arterial catheterization and calculating the left ventricular mass index (LVMI) .The level of serum calcium and nerve phosphatase ( CaN) and the expression of β-myosin heavy chain ( β-MHC) mRNA were detected. Results The thickness of left ventricular,ejection fraction[(69.23± 1.09)% vs(73.77± 3.00)%], fractional shortening [(30.21±2.02)% vs(35.29±0.90)%],LVMI[(2.83±0.14) mg?g-1 vs(2.32±0.11) mg?g-1 ] were decreased,and the differences were statistically significant (P<0.05).The level of serum calcium and nerve phosphatase (CaN) and the expression of β-myosin heavy chain (β-MHC) mRNA were decreased in telmisartan treated rats,and the differences were statistically significant (P< 0.05) when compared with the model control group. Conclusion Telmisartan can improve the myocardial hypertrophy of renovascular hypertensive rats,and it may downregulate the expression of β-MHC by inactivating of the start signal CaN and its downstream signal pathway.
