中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
The Chinese Journal of Clinical Pharmacology
2015年
16期
1622-1625
,共4页
尚福军%王捷频%刘慧%李雪%赵连友
尚福軍%王捷頻%劉慧%李雪%趙連友
상복군%왕첩빈%류혜%리설%조련우
心肌肥厚%炎性细胞因子%抗氧化剂%压力负荷
心肌肥厚%炎性細胞因子%抗氧化劑%壓力負荷
심기비후%염성세포인자%항양화제%압력부하
cardiac hypertrophy%inflammatory cytokines%antioxidant%pressure-overload
目的:观察氮乙酰半胱氨酸( NAC)对心肌肥厚的作用并探讨其与炎性因子表达的关系。方法 SD大鼠随机分为4组,假手术组、模型组、假手术药物组及模型药物组,腹主动脉缩窄法建立压力负荷模型。药物组灌胃 NAC (0.2 g? kg-1? d-1)干预8周。通过组织病理和心脏超声评估心肌的肥厚程度,比色法检测胶原含量,RT-PCR和ELISA法测定炎性细胞因子表达水平,用Fenton原理测定心肌内活性氧( ROS )水平。结果与假手术组比较,模型组大鼠的血压升高,且左室重量指数、心肌细胞内径、胶原含量及左室室壁厚度均明显升高(P<0.05);心肌内的肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6) mRNA和蛋白水平也显著升高( P<0.05)。 NAC干预后,心肌组织的ROS水平明显下降,左室重量指数、胶原含量以及左室室壁厚度均较模型组明显降低( P<0.05)。模型药物组的TNF-α、IL-6 mRNA和蛋白水平均较模型组显著下降(P<0.05);但IL-10蛋白含量与假手术组比较差异不显著。结论 NAC可改善压力负荷大鼠心肌肥厚、抑制促炎性细胞因子表达可能是其重要分子机制之一。
目的:觀察氮乙酰半胱氨痠( NAC)對心肌肥厚的作用併探討其與炎性因子錶達的關繫。方法 SD大鼠隨機分為4組,假手術組、模型組、假手術藥物組及模型藥物組,腹主動脈縮窄法建立壓力負荷模型。藥物組灌胃 NAC (0.2 g? kg-1? d-1)榦預8週。通過組織病理和心髒超聲評估心肌的肥厚程度,比色法檢測膠原含量,RT-PCR和ELISA法測定炎性細胞因子錶達水平,用Fenton原理測定心肌內活性氧( ROS )水平。結果與假手術組比較,模型組大鼠的血壓升高,且左室重量指數、心肌細胞內徑、膠原含量及左室室壁厚度均明顯升高(P<0.05);心肌內的腫瘤壞死因子(TNF-α)、白細胞介素-6(IL-6) mRNA和蛋白水平也顯著升高( P<0.05)。 NAC榦預後,心肌組織的ROS水平明顯下降,左室重量指數、膠原含量以及左室室壁厚度均較模型組明顯降低( P<0.05)。模型藥物組的TNF-α、IL-6 mRNA和蛋白水平均較模型組顯著下降(P<0.05);但IL-10蛋白含量與假手術組比較差異不顯著。結論 NAC可改善壓力負荷大鼠心肌肥厚、抑製促炎性細胞因子錶達可能是其重要分子機製之一。
목적:관찰담을선반광안산( NAC)대심기비후적작용병탐토기여염성인자표체적관계。방법 SD대서수궤분위4조,가수술조、모형조、가수술약물조급모형약물조,복주동맥축착법건립압력부하모형。약물조관위 NAC (0.2 g? kg-1? d-1)간예8주。통과조직병리화심장초성평고심기적비후정도,비색법검측효원함량,RT-PCR화ELISA법측정염성세포인자표체수평,용Fenton원리측정심기내활성양( ROS )수평。결과여가수술조비교,모형조대서적혈압승고,차좌실중량지수、심기세포내경、효원함량급좌실실벽후도균명현승고(P<0.05);심기내적종류배사인자(TNF-α)、백세포개소-6(IL-6) mRNA화단백수평야현저승고( P<0.05)。 NAC간예후,심기조직적ROS수평명현하강,좌실중량지수、효원함량이급좌실실벽후도균교모형조명현강저( P<0.05)。모형약물조적TNF-α、IL-6 mRNA화단백수평균교모형조현저하강(P<0.05);단IL-10단백함량여가수술조비교차이불현저。결론 NAC가개선압력부하대서심기비후、억제촉염성세포인자표체가능시기중요분자궤제지일。
Objective To investigate the effects of N -acetylcystein ( NAC) on the cardiac hypertrophy in pressure -overload rats and the relationship with the expression of inflammatory cytokines.Methods The SD rats were randomly divided into four groups:sham group, model group , drug group in sham and drug group in model.Pressure-overload rat model was established by abdominal aortic coarctation.Rats in drug group were treated with NAC ( 0.2 g? kg-1? d -1 , ig ) for 8 weeks. Cardiac hypertrophy was evaluated by heart histological analysis and echocardiography.The collagen content was determined by chromatome-try.RT-PCR and ELISA were used to determine the expression of in-flammatory cytokines.The production of reactive oxygen species ( ROS) were measured by Fenton reaction.Results Compared with sham rats, blood pressure, left ventricular weight index( LVWI) , myocyte diameter, left ventricular wall thick(LVWT) as well as the collagen content( CC) in model rats significantly elevated ( P <0.05 ) .In model rats treated with NAC, LVWI, LVWT and CC were significantly decreased as well as the production of ROS ( P <0.05 ) . Furthermore, the expression of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)but IL-10 was elevated in myocardium of pressure-o-verload rats, which was inhibited by NAC( P<0.05).NAC had no effects on the expression of IL-10.Conclusion NAC could improve the cardiac hypertrophy induced by pressure-overload.The effects of NAC probably relates to the decrease of pro-inflammatory cytokines expression in rat myocardium.