CAJ | 학술논문

目的：观察预防性应用人参银杏复方制剂对兔缺血再灌注心肌损伤的保护作用，同时探讨其作用机制。方法采用“二线二结”法建立兔心肌急性缺血/再灌注模型，给药组于缺血/再灌注造模前3 d开始行腹腔注射人参银杏复方制剂，每天1次，用量5 ml·kg-1·d-1，最后一次在造模前30 min行腹腔注射，假手术组和缺血/再灌注组注射同等量生理盐水。伊文思蓝-TTC染色测定心肌梗死范围；心肌缺血区取材，采用TUNEL法检测心肌细胞凋亡，免疫组织化学检测Bcl-2、Bax蛋白表达变化。结果人参银杏复方制剂使心肌梗死范围减少约43%，明显抑制了心肌细胞的凋亡，上调了Bcl-2蛋白的表达（P＜0.05），下调了Bax蛋白的表达（P＜0.05）。结论人参银杏复方制剂能明显减轻缺血/再灌注心肌组织损伤，这种保护效应可能与其抑制缺血/再灌注心肌细胞凋亡有关。
목적：관찰예방성응용인삼은행복방제제대토결혈재관주심기손상적보호작용，동시탐토기작용궤제。방법채용“이선이결”법건립토심기급성결혈/재관주모형，급약조우결혈/재관주조모전3 d개시행복강주사인삼은행복방제제，매천1차，용량5 ml·kg-1·d-1，최후일차재조모전30 min행복강주사，가수술조화결혈/재관주조주사동등량생리염수。이문사람-TTC염색측정심기경사범위；심기결혈구취재，채용TUNEL법검측심기세포조망，면역조직화학검측Bcl-2、Bax단백표체변화。결과인삼은행복방제제사심기경사범위감소약43%，명현억제료심기세포적조망，상조료Bcl-2단백적표체（P＜0.05），하조료Bax단백적표체（P＜0.05）。결론인삼은행복방제제능명현감경결혈/재관주심기조직손상，저충보호효응가능여기억제결혈/재관주심기세포조망유관。
Objective To observe the effect of pretreatment with Ginseng-ginkgo compound (GGC) on myocardial ischemia reperfusion injury in rabbits, and to investigate the mechanism. Methods The model of acute myocardial ischemia reperfusion (MIR) injury in rabbits were established by using the two sutures two ligations method. Rabbits (group GGC) received Ginseng-ginkgo compound intraperitoneal injection for 3 days before ischemia reperfusion injury (5 ml·kg-1·d-1), the last injection was at 30 min before modeling. Rabbits (group shame and group MIR) were injected with the same amount of physiological saline. The size of myocardial infarct was determined by Evans blue-TTC staining. Myocardial cell apoptosis of the ischemia area was detected by TUNEL method. Using immunohistochemical method, the expression of Bcl-2, Bax protein were detected. Results Through pretreatment with Ginseng-ginkgo compound, myocardial infarction range was reduced about 43%, myocardium cell apoptosis of the ischemia area was obviously inhibited, the expression of Bcl-2 protein was upregulated (P<0.05), the expression of Bax protein was downregulated (P<0.05). Conclusion Ginseng-ginkgo compound can obviously relieve the ischemia/reperfusion myocardial tissue injury, this protective effect may be related to the inhibition of myocardial cell apoptosis after ischemia/reperfusion.