国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
INTERNATIONAL JOURNAL OF TRIDITIONAL CHINESE MEDICINE
2013年
9期
785-788
,共4页
高血压%心肌肥厚%粉防己碱%血管紧张素Ⅱ%肿瘤坏死因子-α%白细胞介素-1β
高血壓%心肌肥厚%粉防己堿%血管緊張素Ⅱ%腫瘤壞死因子-α%白細胞介素-1β
고혈압%심기비후%분방기감%혈관긴장소Ⅱ%종류배사인자-α%백세포개소-1β
Hypertension%Myocardial Hypertrophy%Tetrandrine%AngiotensinⅡ%TNF-α%IL-1β
目的 探讨粉防己碱对肾性高血压大鼠心肌肥厚的影响及其可能机制.方法 采用两肾一夹型肾性高血压大鼠心肌肥厚模型.手术造模前,所有大鼠被随机分为4组(每组15只):假手术组,高血压模型组,粉防己碱组,和依那普利组.后两组于肾动脉缩窄术后第5周分别给予粉防己碱50 ml/kg·d-1或依那普利6 ml/kg·d-1.采用标准尾套法检测大鼠血压.给药8周后处死大鼠,并检测左心室重/体重以及心肌组织血管紧张素Ⅱ含量和炎症因子TNF-α、IL-1βmRNA表达量.结果 与假手术组[(14.90±3.31)kPa; (1.89±0.27) mg/g; (27.38±7.10) pg/mg; GAPDH表达量的(0.72±0.10)和(0.65±0.10)倍]相比,未给药的高血压模型组大鼠血压[(23.53±3.40) kPa]明显升高,左心室重/体重[(2.83±0.40) mg/g]增大,心肌血管紧张素Ⅱ含量[(43.51±7.37) pg/mg]及TNF-α、IL-1βmRNA表达量[GAPDH表达量的(1.47±0.14)和(1.07±0.11)倍]明显增加.应用粉防己碱治疗则明显降低了2K1C肾性高血压大鼠的血压[(15.81±3.12) kPa]以及左心室重/体重[(1.94±0.31) mg/g],并减少其心肌血管紧张素Ⅱ含量[(31.31±6.69)pg/mg]及TNF-α、IL-1βmRNA表达量[GAPDH表达量的(0.76±0.11)和(0.63±0.09)倍].结论 长时程粉防己碱治疗可抑制肾性高血压大鼠心肌肥厚,其作用机制可能与药物抑制心肌组织局部血管紧张素Ⅱ产生和炎症因子TNF-α、IL-1βmRNA表达作用相关.
目的 探討粉防己堿對腎性高血壓大鼠心肌肥厚的影響及其可能機製.方法 採用兩腎一夾型腎性高血壓大鼠心肌肥厚模型.手術造模前,所有大鼠被隨機分為4組(每組15隻):假手術組,高血壓模型組,粉防己堿組,和依那普利組.後兩組于腎動脈縮窄術後第5週分彆給予粉防己堿50 ml/kg·d-1或依那普利6 ml/kg·d-1.採用標準尾套法檢測大鼠血壓.給藥8週後處死大鼠,併檢測左心室重/體重以及心肌組織血管緊張素Ⅱ含量和炎癥因子TNF-α、IL-1βmRNA錶達量.結果 與假手術組[(14.90±3.31)kPa; (1.89±0.27) mg/g; (27.38±7.10) pg/mg; GAPDH錶達量的(0.72±0.10)和(0.65±0.10)倍]相比,未給藥的高血壓模型組大鼠血壓[(23.53±3.40) kPa]明顯升高,左心室重/體重[(2.83±0.40) mg/g]增大,心肌血管緊張素Ⅱ含量[(43.51±7.37) pg/mg]及TNF-α、IL-1βmRNA錶達量[GAPDH錶達量的(1.47±0.14)和(1.07±0.11)倍]明顯增加.應用粉防己堿治療則明顯降低瞭2K1C腎性高血壓大鼠的血壓[(15.81±3.12) kPa]以及左心室重/體重[(1.94±0.31) mg/g],併減少其心肌血管緊張素Ⅱ含量[(31.31±6.69)pg/mg]及TNF-α、IL-1βmRNA錶達量[GAPDH錶達量的(0.76±0.11)和(0.63±0.09)倍].結論 長時程粉防己堿治療可抑製腎性高血壓大鼠心肌肥厚,其作用機製可能與藥物抑製心肌組織跼部血管緊張素Ⅱ產生和炎癥因子TNF-α、IL-1βmRNA錶達作用相關.
목적 탐토분방기감대신성고혈압대서심기비후적영향급기가능궤제.방법 채용량신일협형신성고혈압대서심기비후모형.수술조모전,소유대서피수궤분위4조(매조15지):가수술조,고혈압모형조,분방기감조,화의나보리조.후량조우신동맥축착술후제5주분별급여분방기감50 ml/kg·d-1혹의나보리6 ml/kg·d-1.채용표준미투법검측대서혈압.급약8주후처사대서,병검측좌심실중/체중이급심기조직혈관긴장소Ⅱ함량화염증인자TNF-α、IL-1βmRNA표체량.결과 여가수술조[(14.90±3.31)kPa; (1.89±0.27) mg/g; (27.38±7.10) pg/mg; GAPDH표체량적(0.72±0.10)화(0.65±0.10)배]상비,미급약적고혈압모형조대서혈압[(23.53±3.40) kPa]명현승고,좌심실중/체중[(2.83±0.40) mg/g]증대,심기혈관긴장소Ⅱ함량[(43.51±7.37) pg/mg]급TNF-α、IL-1βmRNA표체량[GAPDH표체량적(1.47±0.14)화(1.07±0.11)배]명현증가.응용분방기감치료칙명현강저료2K1C신성고혈압대서적혈압[(15.81±3.12) kPa]이급좌심실중/체중[(1.94±0.31) mg/g],병감소기심기혈관긴장소Ⅱ함량[(31.31±6.69)pg/mg]급TNF-α、IL-1βmRNA표체량[GAPDH표체량적(0.76±0.11)화(0.63±0.09)배].결론 장시정분방기감치료가억제신성고혈압대서심기비후,기작용궤제가능여약물억제심기조직국부혈관긴장소Ⅱ산생화염증인자TNF-α、IL-1βmRNA표체작용상관.
Objective To investigate the effects of tetrandrine on myocardial hypertrophy in renohypertensive rats and its possible mechanism.Methods The myocardial hypertrophy models were established in two-kidney-one-clip (2K1C)renovascular hypertensive rats.Before renal artery constriction,all the rats were randomly divided into four groups(n=15 per group):(1) the sham-operated control group; (2) the 2K1C renohypertensive group; (3) the tetrandrine group,the two-kidney-one-clip renohypertensive rats were treated with tetrandrine at a dose of 50 ml/kg · d-1 from the post-operated 5th week; (4) the enapril group,the two-kidney-one-clip renohypertensive rats were treated with enapril at a dose of 6 ml/kg· d-1 from the post-operated 5th week.The standard tail-cuff method was used to measure blood pressure in conscious rats.After drug treatment for 8 weeks,the rats were killed and left ventricle was obtained to measure the ratio of left ventricle weight to body weight (LVW/BW),myocardial angiotensin Ⅱ content,and mRNA expressions of inflammatory cytokines tumor necrosis factor-α(TNF-α)and interleukin-1 β (IL-1β).Results Compared with shamgroup[(14.90±3.31)kPa; (1.89±0.27)mg/g; (27.38±7.10)pg/mg; (0.72±0.10)and(0.65±0.10)fold of GAPDH expression],the untreated 2K1C renohypertensive rats exhibited a significant increase in blood pressure [(23.53 ± 3.40) kPa],LVW/BW [(2.83 ± 0.40) mg/g],angiotensin Ⅱ content [(43.51 ± 7.37) pg/mg],and mRNA expressions of TNF-α and IL-1β [(1.47 ± 0.14) and (1.07 ± 0.11) fold of GAPDH expression].Treatment with tetradrine significantly attenuated the increase in blood pressure [(15.81 ± 3.12) kPa] and LVW/BW [(1.94 ±0.31) mg/g],angiotensin Ⅱ content [(31.31 ± 6.69) pg/mg],and mRNA expressions of TNF-α and IL-1β [(0.76 ±0.11) and (0.63 ± 0.09) fold of GAPDH expression].Conclusion Long-term related to its inhibition of local production or release of angiotensin Ⅱ and inflammatory cytokines TNF-α and IL-1β in the myocardium of renohypertensive rats.
