黄芪甲苷对病毒性心肌炎小鼠心肌纤维化的影响(英文)

Effect of astragaloside on myocardial fibrosis in viral myocarditic mice

目的 :探讨黄芪活性成分黄芪甲苷对小鼠病毒性心肌炎心肌纤维化的影响。方法 :BALB/C小鼠 10 0只 ,随机分成 6组。非感染小鼠腹腔无菌注射病毒培养液 ,分为正常对照组 (A组 ,12只 ,以生理盐水 0 .1mL灌胃 7d)、9%黄芪甲苷对照组(B组 ,16只 ,9%黄芪甲苷 0 .1mL灌胃 7d) ;余 72只小鼠以柯萨奇病毒 (CVB3)腹腔无菌注射制作病毒性心肌炎模型 ,模型小鼠随机分为心肌炎对照组和 1% ,3% ,9%黄芪甲苷干预心肌炎组 ,分别以生理盐水 ,1% ,3%和 9%黄芪甲苷 0 .1mL灌胃 7d (分别为C ,D ,E ,F组 ,每组 18只 )。 14d后处死小鼠 ,以ELISA法检测血清胶原前肽 (PIP和PII INP)浓度 ,心脏组织用天狼星红染色后测定胶原容积积分 (CVF) ,以流式细胞仪检测心肌细胞凋亡指数。结果 :9%黄芪甲苷干预心肌炎组小鼠较心肌炎对照组死亡率明显降低 [2 2 % (4/ 18)vs 4 4%(8/ 18) ,P <0 .0 5 ],9%黄芪甲苷对照组无小鼠死亡 ;与心肌炎对照组相比 ,CVF以及血清PIP和PIIINP浓度在 9%黄芪甲苷干预心肌炎组显著下降 (分别为 (10±s 3) %vs (2 1± 8) % ,(1.4±0 .6 )mg·L- 1vs (3.0± 1.9)mg·L- 1,(2 2± 4 )mg·L- 1vs (2 9± 5 )mg·L- 1,均P <0 .0 1) ,而 1%和 3%黄芪甲苷对心肌炎小鼠生存率和血清胶原前肽无明显影响 ;心肌细胞凋亡指?

AIM: To investigate the effect of astragaloside, one of the active components of Astragalus membranaceus , on myocardial fibrosis in coxsackievirus B 3 (CVB 3) induced murine myocarditis model. METHODS: One hundred BALB/C mice were randomly divided into 6 groups. Group A ( n =12,treated with normal saline 0.1 mL, ig, for 1 wk) was served as normal control and group B ( n =16, treated with 9 % astragaloside 0.1 mL, ig, qd for 1 wk) as treatment control. The seventy two infected animals treated with normal saline (NS) and 1 %, 3 % ,9 % astragaloside 0.1 mL, ig, qd for 1 wk ( n =18 in each group), were served as group C,D,E,F, respectively. The mice were killed after 14 d. Serum concentrations of procollagen peptides (PIP and PIIINP) were measured by ELISA. Collagen volume fraction (CVF) was determined on picrosirius red stained sections with an automated image analysis system. Apoptosis index of cardiac myocytes was measured by flow cytometry. RESULTS: The mortality was significantly reduced in 9 % astragaloside treated infected animals that was 22 %(4/18) vs 44 %(8/18) in group C, P <0.05. In uninfected animals, 9 % astragaloside did not cause any death; CVF and serum procollagen peptides concentrations were significantly lower in group F than that in group C ((10± s 3 ) % vs (21±8) %, (1.4± 0.6) mg·L -1 vs (3.0±1.9) mg·L -1 , (22±4) mg·L -1 vs (29±5) mg·L -1 , respectively, P <0.01). The survival, CVF and serum peptides were not affected by 1 % and 3 % astragaloside. Apoptosis index of cardiac myocytes was lower in 9 % astragaloside treated infected murines compared with that in group C ((13 ±6 ) % vs (36±11) %, P <0.01)).There was a direct correlation between apoptosis index and CVF( r = 0.717, P <0.01), the concentrations of PIP( r = 0.385, P <0.01) and PIIINP( r = 0.391, P <0.01), respectively . CONCLUSION: Results show that 9 % astragaloside can improve survival rate, reduce collagen synthesis and cardiac myocytes apoptosis effectively and safely in this model. The antiapoptotic effect of astragaloside can play an important role for alleviating and reversing myocardial fibrosis.