环球中医药
環毬中醫藥
배구중의약
GLOBAL TCM
2015年
4期
419-423
,共5页
冯玄超%郭淑贞%武志黔%廉洪建%王伟
馮玄超%郭淑貞%武誌黔%廉洪建%王偉
풍현초%곽숙정%무지검%렴홍건%왕위
益心解毒方%慢性心力衰竭%气虚血瘀证%血管新生
益心解毒方%慢性心力衰竭%氣虛血瘀證%血管新生
익심해독방%만성심력쇠갈%기허혈어증%혈관신생
Yixin Jiedu Formula%Chronic heart failure%Qi deficiency and blood stasis syn-drome%Angiogenesis
目的:从血管新生的角度,探讨益心解毒方对气虚血瘀证心衰大鼠心肌保护的作用机制。方法利用左冠状动脉结扎术制备大鼠心梗后心衰动物模型,通过宏观表征判定该疾病模型的证候属性,将成模后存活大鼠随机分为8组:假手术组,模型组,益心解毒方高、中、低剂量组,中西结合组,福辛普利组和芪苈强心组。治疗4周后取梗死边缘区组织进行Western Blot及RT-PCR法检测血小板—内皮细胞黏附分子(又称CD31)和血管内皮生长因子的表达。结果 Western Blot结果显示:模型组大鼠心肌组织中CD31蛋白表达量较假手术组显著下降( P=0.004),而高剂量组(P=0.042)、低剂量组(P=0.027)和芪苈强心组(P=0.015)与模型组相比均可提高心肌组织中CD31的表达。 PCR结果显示:与假手术组相比,大鼠心肌组织的血管内皮生长因子表达在模型组(P=0.047),高剂量(P=0.023),中西结合组(P=0.008)均显著升高;而低剂量组大鼠心肌组织中血管内皮生长因子的表达显著低于模型组(P=0.004)和其它治疗组(P<0.05)。结论益心解毒方对心梗所致气虚血瘀证心衰大鼠的心肌保护作用,可能是通过促进血管新生实现的,其机制可能与血管内皮生长因子有关,且具有剂量相关性。
目的:從血管新生的角度,探討益心解毒方對氣虛血瘀證心衰大鼠心肌保護的作用機製。方法利用左冠狀動脈結扎術製備大鼠心梗後心衰動物模型,通過宏觀錶徵判定該疾病模型的證候屬性,將成模後存活大鼠隨機分為8組:假手術組,模型組,益心解毒方高、中、低劑量組,中西結閤組,福辛普利組和芪藶彊心組。治療4週後取梗死邊緣區組織進行Western Blot及RT-PCR法檢測血小闆—內皮細胞黏附分子(又稱CD31)和血管內皮生長因子的錶達。結果 Western Blot結果顯示:模型組大鼠心肌組織中CD31蛋白錶達量較假手術組顯著下降( P=0.004),而高劑量組(P=0.042)、低劑量組(P=0.027)和芪藶彊心組(P=0.015)與模型組相比均可提高心肌組織中CD31的錶達。 PCR結果顯示:與假手術組相比,大鼠心肌組織的血管內皮生長因子錶達在模型組(P=0.047),高劑量(P=0.023),中西結閤組(P=0.008)均顯著升高;而低劑量組大鼠心肌組織中血管內皮生長因子的錶達顯著低于模型組(P=0.004)和其它治療組(P<0.05)。結論益心解毒方對心梗所緻氣虛血瘀證心衰大鼠的心肌保護作用,可能是通過促進血管新生實現的,其機製可能與血管內皮生長因子有關,且具有劑量相關性。
목적:종혈관신생적각도,탐토익심해독방대기허혈어증심쇠대서심기보호적작용궤제。방법이용좌관상동맥결찰술제비대서심경후심쇠동물모형,통과굉관표정판정해질병모형적증후속성,장성모후존활대서수궤분위8조:가수술조,모형조,익심해독방고、중、저제량조,중서결합조,복신보리조화기력강심조。치료4주후취경사변연구조직진행Western Blot급RT-PCR법검측혈소판—내피세포점부분자(우칭CD31)화혈관내피생장인자적표체。결과 Western Blot결과현시:모형조대서심기조직중CD31단백표체량교가수술조현저하강( P=0.004),이고제량조(P=0.042)、저제량조(P=0.027)화기력강심조(P=0.015)여모형조상비균가제고심기조직중CD31적표체。 PCR결과현시:여가수술조상비,대서심기조직적혈관내피생장인자표체재모형조(P=0.047),고제량(P=0.023),중서결합조(P=0.008)균현저승고;이저제량조대서심기조직중혈관내피생장인자적표체현저저우모형조(P=0.004)화기타치료조(P<0.05)。결론익심해독방대심경소치기허혈어증심쇠대서적심기보호작용,가능시통과촉진혈관신생실현적,기궤제가능여혈관내피생장인자유관,차구유제량상관성。
Objective To clarify myocardial protection mechanism of Yixin Jiedu Formula ( YX-JDF) on chronic heart failure rats with qi deficiency and blood stasis syndrome based on angiogenesis. Methods Rat models of heart failure were established by using left coronary artery ligation. The syn-drome of rats was evaluated by macroscopic symptoms. All the survival rats after model establishment were randomly divided into 8 groups: sham-operated group, model group, high, middle and low dose of YXJDF groups, combination therapy group, fosinopril group and Qili Qiangxin ( QLQX) group. 4 weeks after treatment, western blot and RT-PCR were used to test the expression of CD31 and vascular endothe-lial growth factor ( VEGF) in infarction border zone. Results The results of western blot showed that the expression of CD31 in cardiac muscle tissue of rats in model group was significantly decreased compared with the sham operated group (P=0. 004), while the protein expression of CD31 in myocardial tissue of rats in the high and low dosage of Yixin Jiedu formula group (P=0. 042, P=0. 027) and Qili Qiangxin capsule group (P=0. 015) was increased significantly. The RT-PCR results indicated that, compared with the sham operated group, the expression of VEGF in myocardial tissue of rats in model group ( P=0. 047), high dose of Yiqi Jiedu formula group (P=0. 023) and combination therapy group (P=0. 008) were dramatically increased, while the expression of VEGF in myocardial tissue of rats in low dose of Yiqi Jiedu formula group was lower than that of rats in model group (P=0. 004) and the other treat-ment groups (P<0. 05). Conclusion Yixin Jiedu formula could protect the cardiac muscle of rats with qi deficiency and blood stasis syndrome induced by myocardial infarction through promoting angiogenesis possibly, and the mechanism might be relate to VEGF family, and the protective effect changes with dif-ferent doses.